Effect of partial pressure of reactive gas on chromium nitride and chromium oxide deposited by

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枸橼酸咖啡因注射液联合猪肺磷脂注射液治疗新生儿呼吸窘迫综合征的临床研究

枸橼酸咖啡因注射液联合猪肺磷脂注射液治疗新生儿呼吸窘迫综合征的临床研究

- 47 -①广州市白云区妇幼保健院新生儿科 广东 广州 510400通信作者:高颖博枸橼酸咖啡因注射液联合猪肺磷脂注射液治疗新生儿呼吸窘迫综合征的临床研究高颖博① 包莉娜① 蒋琼① 冯国仙①【摘要】 目的:探讨新生儿呼吸窘迫综合征联合应用枸橼酸咖啡因注射液、猪肺磷脂注射液治疗的效果。

方法:抽取广州市白云区妇幼保健院2018年3月—2023年3月收治的新生儿呼吸窘迫综合征90例为研究对象,采用随机数字表法分为对照组和试验组,各45例,对照组行猪肺磷脂注射液治疗,试验组行枸橼酸咖啡因注射液+猪肺磷脂注射液治疗,观察两组动脉血气指标、炎症因子变化情况,并评估两组治疗效果及安全性。

结果:(1)试验组治疗总有效率显著高于对照组,差异有统计学意义(P <0.05);(2)试验组治疗后氧分压(PaO 2)、二氧化碳分压(PaCO 2)、血氧饱和度(SaO 2)、氢离子浓度指数(pH)水平均显著优于对照组,差异均有统计学意义(P <0.05);(3)试验组治疗后白细胞介素-6(IL-6)、降钙素原(PCT)、C 反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)水平均显著低于对照组,差异均有统计学意义(P <0.05);(4)试验组不良反应总发生率与对照组比较,差异无统计学意义(P >0.05)。

结论:针对新生儿呼吸窘迫综合征,予以枸橼酸咖啡因注射液+猪肺磷脂注射液治疗,可改善动脉血气,减轻机体炎症反应,提高疗效,且联合用药不增加不良反应发生率。

【关键词】 新生儿呼吸窘迫综合征 枸橼酸咖啡因注射液 猪肺磷脂注射液or ⅡB squamous cervical cancer:a randomized controlled trial[J].Journal of Clinical Oncology,2018,36(16):1548-1555.[8] DA COSTA S C S,BONADIO R C,GABRIELLI F C G,et al. Neoadjuvant chemotherapy with Cisplatin and Gemcitabine followed by chemoradiation versus chemoradiation for locally advanced cervical cancer:a randomized phase Ⅱ trial[J].Journal of Clinical Oncology,2019,37(33):3124-3131.[9] TEWARI K S,MONK B J,VERGOTE I,et al.Survival with cemiplimab in recurrent cervical cancer[J].New England Journal of Medicine,2022,386(6):544-555.[10]杜银萍,贾雪梅.常规放疗与调强放射治疗对中晚期宫颈癌患者复发率及转移率的影响[J].临床与病理杂志,2022,42(1):73-80.[11]汤红,张彪,周龙兰.参麦注射液联合卡培他滨治疗结肠癌晚期患者疗效观察及对免疫功能的影响[J].湖北中医药大学学报,2021,23(5):35-37.[12]张淑平,王迎春.参麦注射液对乳腺癌术后化疗患者心肌功能和免疫功能的影响[J].中国医院用药评价与分析,2020,20(2):214-217.[13]赵丽萍,陈勇,徐益元,等.参麦注射液治疗对肺癌化疗患者免疫功能的影响[J].新中医,2021,53(24):137-140.[14]叶传素,张月群,殷凯铃,等.揿针中医干预联合五音疗法对早孕药物流产患者镇痛效果的影响[J].齐鲁护理杂志,2023,29(1):42-45.[15]李丹,卢道珍.基于“心-肾-子宫轴”理论的揿针留针候气对加速康复外科宫颈癌术后胃肠功能恢复的研究[J].饮食保健,2021(37):131-132.[16]李强,于晓霞,范志刚.高强度超声介入治疗对宫颈癌小鼠模型肿瘤增殖、免疫功能及脾细胞Th1/Th2亚群的影响[J].临床和实验医学杂志,2023,22(1):1-4.[17]薛彩琴,颜红丽,任晋林,等.紫杉醇联合卡铂治疗中晚期宫颈癌的临床疗效及对患者免疫功能和生活质量的影响[J].癌症进展,2022,20(17):1802-1805.[18]宋洪杰.八珍汤加减联合穴位艾灸对放化疗子宫颈癌患者免疫水平及生存质量的影响研究[J].中国医学创新,2022,19(21):82-86.[19]肖婷婷,肖黎丽,徐敏娟,等.四关四穴穴位贴敷对宫颈癌患者化疗后癌因性疲乏的影响[J].中文科技期刊数据库(引文版)医药卫生,2022(4):60-63.[20] ZUSTERZEEL P L M,AARTS J W M,POL F J M,et al.Neoadjuvant chemotherapy followed by vaginal radical trachelectomy as fertility-preserving treatment for patients with FIGO 2018 stage 1B2 cervical cancer[J/OL].The Oncologist,2020,25(7):e1051-e1059.https:///32339376/.(收稿日期:2023-09-20) (本文编辑:陈韵) 因缺乏肺表面活性物质致肺泡萎陷,新生儿出生数小时后出现呼吸困难、发绀等表现,称为新生儿呼吸窘迫综合征[1]。

黄芪阳和汤调控PI3K

黄芪阳和汤调控PI3K

实验研究黄芪阳和汤调控PI3K/AKT/NF-κB信号通路促进糖尿病足溃疡大鼠创面愈合鲍亚玲1,雷慧1△,马君2,赵新梅2摘要:目的 基于磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)/核因子-κB(NF-κB)信号通路探究黄芪阳和汤对糖尿病足溃疡(DFU)大鼠创面愈合的影响。

方法 构建DFU大鼠模型,将建模成功的48只大鼠随机分为模型组,黄芪阳和汤低(8.5 g/kg)、高(17 g/kg)剂量组,黄芪阳和汤高剂量(17 g/kg)+LY294002(PI3K/AKT通路抑制剂,0.3 mg/kg)组;每组12只;另取12只大鼠为对照组。

各组大鼠给予对应药物干预,连续4周。

第14、28天给药后,观察大鼠一般状态及创面变化,计算创面愈合率,检测大鼠空腹血糖(FBG)水平和大鼠创面周围组织经皮氧分压(TcpO2);酶联免疫吸附试验检测大鼠血清血管内皮生长因子(VEGF)、缺氧诱导因子-1α(HIF-1α)、C反应蛋白(CRP)、白细胞介素(IL)-6水平;苏木素-伊红染色观察大鼠创面组织病理学变化;免疫组织化学染色测定大鼠创面组织微血管密度;蛋白免疫印迹法检测大鼠创面组织中PI3K、磷酸化PI3K(p-PI3K)、AKT、磷酸化AKT(p-AKT)、NF-κB p65、磷酸化NF-κB p65(p-NF-κB p65)、NF-κB抑制蛋白α(IκB-α)蛋白表达。

结果 对照组大鼠毛色光滑,饮食、饮水、排泄均正常,较活跃,创面愈合快,创面组织炎症反应较轻,新生血管较多,肉芽组织中成纤维细胞及胶原基质丰富;模型组大鼠毛色暗淡无光泽,活动减少,且出现多饮、多食、多尿症状,创面颜色较深,且周围组织出现水肿、溃疡,创面组织可见大量炎性细胞浸润,伴组织坏死、渗出,新生血管及成纤维细胞较少,创面愈合率、创面周围组织TcpO2、血清VEGF、HIF-1α、创面组织微血管密度、p-PI3K、p-AKT、IκB-α蛋白表达水平降低,FBG、血清CRP、IL-6、创面组织p-NF-κB p65蛋白表达升高(P<0.05);与模型组相比,黄芪阳和汤低、高剂量组大鼠状态逐渐改善,创面组织病变程度依次减轻,创面愈合率、创面周围组织TcpO2、血清VEGF、HIF-1α、创面组织微血管密度、p-PI3K、p-AKT、IκB-α蛋白表达水平依次升高,FBG、血清CRP、IL-6、创面组织p-NF-κB p65蛋白表达依次降低(P<0.05);LY294002能部分逆转高剂量黄芪阳和汤对DFU大鼠的治疗作用(P<0.05)。

纤支镜对重症肺部感染患者炎症因子水平、血气指标与肺功能指标的影响

纤支镜对重症肺部感染患者炎症因子水平、血气指标与肺功能指标的影响

DOI:10.16662/ki.1674-0742.2023.20.048纤支镜对重症肺部感染患者炎症因子水平、血气指标与肺功能指标的影响万展鸥,郭永明,黄浩福建医科大学临床医学部/福建省老年医院,福建福州350003[摘要]目的研究纤维支气管镜(纤支镜)对重症肺部感染患者炎症因子水平、血气指标与肺功能指标的影响。

方法随机选取2020年1月—2022年12月福建省老年医院收治的80例重症肺部感染患者作为研究对象,随机分为对照组40例,采用常规治疗;研究组40例,采用常规治疗+纤支镜治疗。

统计两组临床疗效、退热时间、呼吸机辅助时间、呼吸衰竭纠正时间及治疗前后的炎症因子水平、血气指标与肺功能指标。

结果研究组治疗总有效率为100.00%,高于对照组的85.00%,退热时间、呼吸机辅助时间、呼吸衰竭纠正时间短于对照组,差异有统计学意义(χ2=4.505,t=11.187、10.424、8.311,P<0.05)。

结论纤支镜可提高重症肺部感染的效果,缩短退热、呼吸机辅助及呼吸衰竭纠正时间,降低炎症因子,改善血气指标及肺功能情况。

[关键词]纤支镜;重症肺部感染;炎症因子;血气指标;肺功能[中图分类号]R5 [文献标识码]A [文章编号]1674-0742(2023)07(b)-0048-05Effects of Fiberoptic Bronchoscopy on Inflammatory Factor Levels, Blood Gas Indexes and Lung Function Indexes in Patients with Severe Pulmo⁃nary InfectionWAN Zhan'ou, GUO Yongming, HUANG HaoDepartment of Clinical Medicine, Fujian Medical University / Fujian Provincial Geriatric Hospital, Fuzhou, Fujian Province, 350003 China[Abstract] Objective To study the effects of bronchofiberscope (bronchobronchoscope) on the levels of inflammatory factors, blood gas indexes and lung function indexes in patients with severe pulmonary infection. Methods A total of 80 patients with severe pulmonary infection admitted to the Fujian Provincial Geriatric Hospital from January 2020 to December 2022 were randomly selected as the study objects, and randomly divided into control group (40 cases) with conventional treatment, and study group (40 cases) with conventional treatment and bronchoscopy. The clinical effi⁃cacy, fever reduction time, ventilator assistance time, expiratory failure correction time, levels of inflammatory factors before and after treatment, blood gas index and lung function index of the two groups were analyzed. Results The total effective rate of the study group was 100.00%, which was higher than that of the control group 85.00%, and the time of fever reduction, ventilator assistance and expiratory failure correction were shorter than those of the control group, the difference was statistically significant (χ2=4.505, t=11.187, 10.424, 8.311, P<0.05). Conclusion Fiberoptic bronchos⁃copy can improve the effect of severe pulmonary infection, shorten the time of fever reduction, ventilator assistance and expiratory failure correction, reduce inflammatory factors, improve blood gas indexes and lung function.[Key words] Fiberoptic bronchoscopy; Severe pulmonary infection; Inflammatory factors; Blood gas index; Lung function重症肺部感染是一种急危重症,具有较高的发病率,多因致病性较强或多种致病菌混合感染造[作者简介] 万展鸥(1985-),男,本科,主治医师,研究方向为急诊医学。

心血管常用英文缩写

心血管常用英文缩写

心血管常用缩写AA2 aortic second sound 主动脉区第二音AA amino acid 氨基酸AAA abdominal aortic aneurysm 腹主动脉瘤Ab antibody 抗体ABE acute bacterial endocarditis 急性细菌性心膜炎ABG arterial blood gases 动脉血气ABI ankle brachial inde* 踝肱指数ABP arterial blood pressure 动脉血压ABPM ambulatory blood pressure monitoring 动态血压监测AC alternating current 交流电AC aortic closure 动脉闭锁ACAT acyl CoA:cholesterol acyltransferase 胆固醇酰基转移酶ACE angiotensin converting enzyme 血管紧素转化酶ACEI angiotensin converting enzyme inhibitors 血管紧素转化酶抑制剂ACG angiocardiography 心血管造影术ACh acetylcholine 乙酰胆碱ACS acute coronary syndromes 急性冠状动脉综合症ACTH adrenocorticotropic hormone 促肾上腺皮质激素ADH antidiuretic hormone 抗利尿激素ADP adenosine diphosphate 二磷酸腺苷AECG ambulatory electrocardiography 动态心电图AEDs automatic e*ternal defibrillators 自动体外除颤器AF atrial fibrillation 房颤AFL atrial flutter 心房扑动AG atrial gallop 心房性奔马律AHA American Heart Association 美国心脏协会AHP apical hypertrophy 心尖部肥厚AI aortic inpetence 主动脉瓣关闭不全AI aortic insufficiency 主动脉瓣功能不全AI apical impulse 心尖搏动AICD automatic implantable cardioverter-defibrillator 埋藏式自动心脏复律除颤器AICDS automatic implanted cardioverter defibrillators 自动植入式心脏复律除颤器AIDS acquired immunodeficiency syndrome 爱滋病AIVR Accelerated idioventricular rhythm 加速性心室自主节律ALT alanine aminotransferase 丙氨酸氨基转移酶AMI acute myocardial imfarction 急性心肌堵塞AML anterior mitral valve leaflet 二尖瓣前叶ANA antinuclear antibody 抗核抗体ANCA antineutrophilic cytoplasmic antibodies 抗中性粒细胞胞浆抗体ANGII angiotensin II 血管紧素IIANOVA analysis of variance 方差分析ANP atrial natriuretic hormone 心房利钠激素ANP atrial natriuretic peptide 心房利钠肽ANS autonomic nervous system 自主神经系统Ao aorta 主动脉AO opening of the atrioventricular valves 房室瓣开AoP aortic pressure 主动脉压力AP accessory pathway 旁路AP action potential 动作电位AP angina pectoris 心绞痛AP arterial pressure 动脉压APB atrial premature beat 房性早搏APC atrial premature ple* 房性早搏APH apical hypertrophy 心尖部肥厚APA action potential amplitude 动作电位幅度APC activated protein C 活化的蛋白CAPD action potential duration 动作电位时间apoA apolipoprotein A 载脂蛋白AapoB apolipoprotein B 载脂蛋白BaPPT actived partial thromboplastin time 激活的局部凝血活酶时间APSAC anisolysated plasminogen streptokinase activated ple* 苯甲氧酰纤溶酶原链激酶活化复合物AR aortic regurgitation 主动脉瓣关闭不全AR alarm reaction 应激反响AR artificial respiration 人工呼吸ARDS adult respiratory distress syndrome 成人呼吸窘迫综合症Arg arginine 精氨酸ARP atrial refractory period 心房不应期ARVD arrhythmogenic right ventricular dysplasia 致心律失常性右心室发育不良AS aortic stenosis 主动脉瓣狭窄AS arteriosclerosis 动脉硬化ASCVD arteriosclerotic cardiovascular disease 动脉粥样硬化性心血管病ASD atrial septal defect 房间隔缺损ASH asymmetric septal hypertrophy 非对称性心室间隔肥厚ASHD arteriosclerotic heart disease 动脉硬化性心脏病ASO anti-streptolysin "O" 抗链球菌溶血素OASO arteriosclerosis obliterans 闭塞性动脉硬化AST aspartate aminotransferase 天门冬氨酸氨基转移酶AT angiotensin Ⅱ receptor 血管紧素Ⅱ受体AT atrial tachycardia 房性心动过速AT-Ⅲ:A antithrombin Ⅲ activity 抗凝血酶Ⅲ活性ATP adenosine triphosphate 三磷酸腺苷ATP antitachycardia pacing 抗心动过速起搏ATPase adenosinetriphosphatase 三磷酸腺苷酶AVA-V atrioventricular 房室性的AVN atrioventricular node 房室结AVNRT atrioventricular nodal reentrant tachycardia 房室结折返性心动过速AVO atrioventricular orifice 房室口AVP arginine vasopressin 精氨酸加压素AVR aortic valve replacement 主动脉瓣置换术AVRT atrioventricular reciprocating tachycardia 房室交互性心动过速BBBB blood-brain barrier 血脑屏障BBB bundle branch block 束支传导阻滞BBBB bilateral bundle branch block 双侧束支传导阻滞BBT basal body temperature 根底体温BDS biodegradable stents 生物可降解支架BFP biologic false-positive 生物学假阳性BLS basic life support 根底生命支持BMI body mass inde* 体质指数BMR basal metabolic rate 根底代率BNP brain natriuretic peptide 脑钠肽BUN blood urea nitrogen 尿素氮BP blood pressure 血压BPV blood pressure variability 血压波动性BRF renal blood flow 肾血流B.S. breath sounds 呼吸音B.S. blood sugar 血糖BSA body surface area 体外表积BUN blood urea nitrogen 血尿素氮BVAD biventricular assist device 两心室辅助装置CCA cardiac arrest 心脏停搏CA coronary artery 冠状动脉CA catecholamine 儿茶酚胺C.A. circumfle* coronary artery 左盘旋支冠状动脉CABG coronary artery bypass grafting 冠状动脉旁路移植术CABS coronary artery bypass surgery 冠状动脉分流术CAD coronary artery disease 冠状动脉疾病CAMP cyclic adenosine monophosphate 环磷酸腺苷CAVB plete atrioventricular block 完全房室传导阻滞CBC plete blood count 全血细胞计数CBF cerebral blood flow 脑血流量CC chief plaint 主诉CCPR cardiopulmonary-cerebral resuscitation 心肺脑复CCU coronary care unit 冠心病监护病房CCU critical care unit 危症监护病房CD curative dose 有效量治疗量CDC Centers for Disease Control and Prevention 疾病预防控制中心CEA carcinoembryonic antigen 癌胚抗原CEI cardiac effort inde* 心脏负荷指数CETP cholesteryl ester transfer protein 胆固醇酯转移蛋白CF cardiac failure 心力衰竭CFR coronary flow reserve 冠状动脉血流储藏cGMP cyclic guanosine monophosphate 环-磷酸鸟苷CHD coronary heart disease 冠心病CHF congestive heart failure 充血性心力衰竭CHO Chinese hamster ovary (cell) 中国仓鼠卵巢细胞CI cardiac inde* 心脏指数CIC circulating immune ple* 循环免疫复合物CIE counterimmunoelectrophoresis 对流免疫电泳CK creatine kinase 肌酸激酶CK-BB creatine kinase with brain subunits 肌酸激酶BB亚单位CK-MB creatine kinase-MB 肌酸激酶MB亚单位CK-MM creatine kinase with muscle subunits 肌酸激酶MM亚单位CM chylomicron 乳糜微粒CMLC cardiac myosin light chains 心脏肌凝蛋白轻链CMT circus movement tachycardia 环形运动性心动过速S central nervous system 中枢神经系统CO cardiac output 心输出量CoA coenzyme A 辅酶ACOPD chronic obstructive pulmonary disease 慢性阻塞性肺病CPB cardiopulmonary bypass 体外循环CPAP continuous positive airway pressure 持续气道正压呼吸CPC clinicopathological conference 临床病历讨论会CPK creatine phosphokinase 磷酸肌酸激酶CPK-MB MB fraction of creatine phosphokinase 磷酸肌酸激酶同功酶MBCPR cardiopulmonary resuscitation 心肺复CRH corticotropin-releasing hormone 促肾上腺皮质激素释放激素CRP C-reactive protein C反响蛋白CRT cardiac resynchronization therapy 心脏再同步治疗CS coronary sinus 冠状窦CSF colony-stimulating factor 集落刺激因子CSF cerebrospinal fluid 脑脊液CSM carotid sinus massage 颈动脉窦按摩CSNRT corrected SNRT 校正的窦房结恢复时间CT clotting time 凝血时间CT puted Tomography 计算机体层X线摄影CTA CT angiography CT血管造影cTnI cardiac troponin I 心肌肌钙蛋白IcTnT cardiac troponin T 心肌肌钙蛋白TCTO chronic total occlusion 慢性闭塞病变CV cardiovascular 心血管的CVA cerebrovascular accident 脑血管意外CVD cardiovascular disease 心血管疾病CVP central venous pressure 中心静脉压CVS cardiovascular system 心血管系统DDAD delayed afterdepolarization 延迟后去极化D.A.H disordered action of heart 心功能失调DBP diastolic blood pressure 舒压DC direct-current 直流电DCM dilated cardiomyopathy 扩性心脏病DHEA-S dehydroepiandrosterone sulfate 硫酸脱氢异雄酮DHF diastolic heart failure 舒性心力衰竭DIC disseminated intravascular coagulation 弥漫性血管凝血DL diffusion capacity 弥散量DM diabetes mellitus 糖尿病DM diastolic murmur 舒期杂音DNA deo*yribonucleic acid 脱氧核糖核酸DNR do not resuscitate 不复DOA dead on arrival 到达时已死亡DOC deo*ycorticosterone 脱氧皮质酮DSA digital subtraction angiography 数字减影血管造影术dsDNA double-stranded DNA 双链脱氧核糖核酸DTPA diethylenetriaminepentaacetic acid 二乙烯三胺五乙酸DVT deep venous thrombosis 深静脉血栓形成EEAD early afterdepolarization 早期后除极EAVNC enhanced A-V nodal conduction 房室结加速传导EBV Epstein-Barr virus EB病毒ECC e*ternal chest pression 胸外心脏按压ECG electrocardiogram 心电图ECMO e*tracorporeal membrane o*ygenation 体外循环膜氧合ECS electrocerebral silence 脑电静止ECS endocannabinoid system 分泌大麻系统ED emergency department 急诊室ED effective dose 有效剂量EDCFs endothelium-derived constricting factor 皮衍生的收缩因子EDHF endothelium-derived hyperpolarizing factor 皮衍生超极化因子EDRF endothelium-derived rela*ing factor 皮衍生的松弛因子EDV end-diastolic volume 舒末期容积EERP e*tended endocardial resection procedure 心膜伸展切除法EEV encircling endocardial ventriculotomy 心膜面心室环切术EF ejection fraction 射血分数EKG electrocardiogram 心电图ELISA enzyme-linked immunosorbent assay 酶联免疫吸附试验EMD electromechanical dissociation 电机械别离EMS emergency medical service 急救医疗效劳ERBF effective renal blood flow 有效肾血流量EPS electrophysiology study 电生理检查EPSP e*citatory postsynaptic potential 兴奋性突触后电位ER endoplasmic reticulum 质网ERBF effective renal blood flow 有效肾血流量ERP effective refractory period 有效适应期ERP endocardial resection procedure 心膜切除术ERT estrogen replacement therapy 雌激素替代疗法ERV e*piratory reserve volume 补呼气容积ES cells Embryonic stem cells 胚胎干细胞ESR erythrocyte sedimentation rate 血细胞沉降率ESRD end-stage renal disease 终末期肾脏疾病ESV end-systolic volume 收缩末期容积ET e*citability threshold 兴奋性阈值ET endothelin 皮素FFab fragmentantigen-binding 抗原结合片断FABP fatty acid binding protein 脂肪酸结合蛋白FBG fasting blood glucose 空腹血糖FDP fibrinogen degradation products 纤维蛋白原降解产物FEV1.0 forced e*piratory volume in one second 第1秒用力呼气容积FFA free fatty acid 游离脂肪酸FGF fibroblast growth factor 纤维母细胞生长因子FH familial hypercholesterolemia 家族性高胆固醇血症FHC familial hypertrophic cardiomyopathy 家族性肥厚型心肌病FIO2 fraction of inspired o*ygen 吸入气氧分数FML flail mitral leaflet 连枷样瓣叶FRC functional residual capacity 功能残气量FT3 free triiodothyronine 游离型T3FT4 free thyro*ine 游离型甲状腺素FUO fever of undetermined origin 不明原因发热FVC forced vital capacity 用力肺活量GGAD glutamic acid decarbo*ylase 谷氨酸脱羧酶GAP GTPase-activating protein GTP酶活化蛋白GBM glomerular basement membrane 肾小球基底膜G-CSF granulocyte colony-stimulating factor 粒细胞集落刺激因子GFR glomerular filtration rate 肾小球滤过率GHb glycosylated hemoglobin 糖化血红蛋白GI gastrointestinal 胃肠的GIK glucose_insulin_potassium 葡萄糖-胰岛素-钾〔极化液〕GITS the gastrointestinal therapeutic system 胃肠道治疗系统GMP guanosine monophosphate 一磷酸鸟苷GPBB glycogen phosphorylase isoenzyme 糖原磷酸化酶同工酶BB GPT glutamic-pyruvic transaminase 谷丙转氨酶GTP guanosine triphosphate 三磷酸鸟苷GTT glucose tolerance test 葡萄糖耐量试验HHAV hepatitis A virus 甲肝病毒Hb hemoglobin 血红蛋白HbA1c Hemoglobin A1c 糖化血红蛋白A1cHBcAg hepatitis B core antigen 乙肝核心抗原HBeAg hepatitis B e antigen 乙肝e抗原HBsAg hepatitis B surface antigen 乙肝e抗原HBE His bundle electrogram 希氏束电图HBV hepatitis B virus 乙肝病毒HbO2 o*yhemoglobin 氧合血红蛋白HCM hypertrophic cardiomyopathy 肥厚型心肌病HCT hematocrit 血细胞比容,红细胞压积HDL-C high-density lipoprotein cholesterol 高密度脂蛋白胆固醇HERG Human Ether-a-go-go-Related Gene 人类eag相关基因HF heart failure 心力衰竭hFABP heart fatty acid binding protein 心脏脂肪酸结合蛋白HIT heparin-induced thrombocytopenia 肝素导致的血小板减少症HIV human immunodeficiency virus 人类免疫缺陷病毒HLHS hypoplastic left heart syndrome 左心发育不良综合征HMG-COA 3-hydro*y-3-methylglutaryl coenzyme A 3羟甲基戊二酰辅酶AHMWK high molecular weight kininogen 高分子量激肽原HOCM hypertrophic obstructive cardiomyopathy 肥厚梗阻性心肌病HOP high o*ygen pressure 高压氧HP haptoglobin 结合珠蛋白,触珠蛋白HPI history of the present illness 现病史HPS His-Purkinje system 希氏束-浦肯野系统HR heart rate 心率HRV heart rate variability 心率变异性HuIFN human interferon 人体干扰素IIAB intraaortic balloon 主动脉气囊IABP intraaortic balloon pump 主动脉气囊泵IC inspiratory capacity 深吸气量ICD implantable cardioverter-defibrillator 埋藏式心脏复律-除颤器ICU intensive care unit 重症监护病房IDD insulin-dependent diabetes 胰岛素依赖性糖尿病IDL intermediate-density lipoprotein 中间密度脂蛋白IE infective endocarditis 感染性心膜IFG impaired fasting glucose 空腹血糖调节受损IFN interferon 干扰素IGF-1 insulin-like growth factor-1 胰岛素样生长因子-1IGT impaired glucose tolerance 葡萄糖耐量降低IHD ischemic heart disease 缺血性心脏病IHR intrinsic heart rate 固有心率IHSS idiopathic hypertrophy subaortic stenosis 特发性肥厚型主动脉瓣下狭窄IHUT isoproterenol-head-up tilt testing 异丙肾上腺素-倾斜试验IMA internal mammary artery 乳动脉INR international normalized ratio 国际标准化比值IPG impedance plethysmography 阻抗容积描记法IPPB intermittent positive pressure breathing 间歇性正压呼吸IR insulin resistance 胰岛素抵抗IRMS insulin resistance metabolic syndrome 胰岛素抵抗代综合征IRS insulin resistance syndrome 胰岛素抵抗综合征IRV inspiratory reserve volume 补吸气容积ISA intrinsic sympathomimetic activity 源性拟交感活性IU international unit 国际单位IV intravenously 静脉注射IVC inferior vena cava 下腔静脉IVP intravenous pyelography 静脉肾盂造影IVRT isovolumic rela*ation time 等容舒时间IVS interventricular septum 室间隔IVST interventricular septal thickness 室间隔厚度IVUS intravascular ultrasound 血管超声JJ joule 焦耳KKD Keshan disease 克山病LLA left arm 左臂LA left atrium 左心房LAD left anterior descending (coronary artery) 冠状动脉左前降支LAD left a*is deviation 电轴左偏]LADA latent autoimmune diabetes in adult 成人隐匿自身免疫糖尿病LAE left atrial enlargement 左心房扩大LAFB left anterior fascicular block 左前分支阻滞LAH left anterior hemiblock 左前分支阻滞LAO left anterior oblique 左前斜位LAP left atrial pressure 左心房压力LAPB left anterior parietal block 左前分支末梢阻滞LATS long-acting thyroid stimulator 长效甲状腺刺激素LBBB left bundle branch block 左束支传导阻滞LCA left coronary artery 左冠状动脉LCAT lecithin :cholesterol acyltransferase 卵磷脂胆固醇酰基转移酶LC* left circumfle* artery 左冠状动脉盘旋支LDH lactate dehydrogenase 乳酸脱氢酶LDL-C low-density lipoprotein cholesterol 低密度脂蛋白胆固醇LF left leg 左腿LP(α) α-lipoprotein α脂蛋白LPFB left posterior fascicular block 左后分支阻滞LPH left posterior hemiblock 左后半阻滞LPL lipoprotein lipase 脂蛋白酯酶LQ-T1 long Q-T locus 1 长Q-T位点1LQTS long QT syndrome 长QT综合症LRL lower rate limit 下限频率LV left ventricle 左心室LVAD left ventricular assist device 左室辅助装置LVEDP left ventricular end-diastolic pressure 左室舒末压LVEDV left ventricular end-diastolic volume 左室舒末容积LVET left ventricular ejection time 左心室射血时间LVH left ventricular hypertrophy 左室肥厚LVMI left ventricular mass inde* 左室重量指数MMAF macrophage activating factor 巨噬细胞活化因子MAG3 mercaptoacetyltriglycine 巯基乙酰三甘氨酸MAO monoamine o*idase 单胺氧化酶MAOI monoamine o*idase inhibitor 单胺氧化酶抑制剂MAP mean arterial pressure 平均动脉压MAPK mitogen-actived protein kinase 有丝分裂激活的蛋白激酶MAT multifocal atrial tachycardia 多源性房性心动过速MBC minimum bactericidal concentration 最小杀菌浓度MB-CK MB creatine kinase 肌酸磷酸激酶MB亚单位MCE myocardial contrast echocardiography 心肌造影超声心动图MCF macrophage chemotactic factor 巨噬细胞趋化因子MCH mean corpuscular hemoglobin 红细胞平均血红蛋白量MCHC mean corpuscular hemoglobin concentration 红细胞平均血红蛋白浓度MCT mean circulation time 平均循环时间MCV mean corpuscular volume 平均红细胞容积MDF myocardial depressant factor 心肌抑制因子MDP ma*imum diastolic potential 最大舒电位MEN multiple endocrine neoplasia 多发性分泌肿瘤METS multiple of basal metabolic o*ygen consumption 根底代氧消耗倍数MHC myosin heavy chain 肌球蛋白重链MI myocardial imfarction 心肌堵塞MIC minimum inhibitory concentration 最小抑菌浓度MLC myosin light chain 肌凝蛋白轻链MMD minor myocardial damage 微小心肌损伤MODS multiple organ dysfunction syndrome 多脏器功能障碍综合征MPD ma*imum permissible dose 最大允许剂量MPS mononuclear phagocyte system 单核巨噬细胞系统MPS mucopolysaccharidosis 粘多糖〔贮积〕病MR mitral regurgitation 二尖瓣关闭不全MRA magnetic resonance angiography 核磁共振血管造影MRI magnetic resonance imaging 核磁共振显像mRNA messenger RNA 信使核糖核酸MS metabolic syndrome 代综合征MS mitral stenosis 二尖瓣狭窄MSCT multi-slice puted tomography 多层螺旋CTMSCTCA MSCT coronary angiography 多层螺旋CT冠状动脉造影MSL midsternal line 胸骨中线MV mitral valve 二尖瓣MVO2 myocardial o*ygen requirements 心肌需氧量MVP mitral valve prolapse 二尖瓣脱垂MVV ma*imal voluntary ventilation 最大自主通气量NNBTE nonbacterial thrombotic endocarditis 非细菌性血栓性心膜炎NED no evidence of disease 无疾病证据NEFA nonesterified fatty acids 非酯型脂肪酸游离脂肪酸NEP neutral endopeptidase 中性肽酶NIDD non-insulin-dependent diabetes 非胰岛素依赖性糖尿病NMR nuclear magnetic resonance 核磁共振NO nitric o*ide 一氧化氮NPN nonprotein nitrogenNQWMI non-Q-wave myocardial infarction 非Q波心肌堵塞NSAIA nonsteroidal anti-inflammatory analgesic 非类固醇消炎止痛药NSAIDs nonsteriodal anti-inflammatory drugs 非甾族抗炎药物NSR normal sinus rhythm 正常窦律NTP normal temperature and pressure 正常体温与血压NVE native valve endocarditis 自身瓣膜心膜炎NYHA New York Heart Association 纽约心脏协会OOMB obtuse marginal branch 钝缘支OR operating room 手术室OS opening snap 开放拍击音OSAS obstructive sleep apnea syndrome 阻塞性睡眠呼吸暂停综合征OTC over the counter 非处方药物OTD organ tolerance dose 器官耐受剂量(*线)PP2 pulmonic second sound 肺动脉第二心音PA posteroanterior 后前位的PA pulmonary artery 肺动脉PAC premature atrial ple* 期前心房复合波PAF platelet-activating factor 血小板激活因子PAI-1 plasminogen activator inhibitor-1 纤维蛋白酶原激活物抑制剂-1PAP plasmin-antiplasmin ple* 纤溶酶抗纤溶酶复合物PAT paro*ysmal atrial tachycardia 阵发性房性心动过速PAWP pulmonary artery wedge pressure 肺动脉楔压力PBAV percutaneous balloon aortic valvuloplasty 经皮球囊主动脉瓣成形术PBMV percutaneous balloon mitral valvuloplasty 经皮球囊二尖瓣成形术PBPV percutaneous balloon pulmonary valvuloplasty 经皮球囊肺动脉瓣成形术PC:A protein C activity 蛋白C活性PCG phonocardiogram 心音图PCI percutaneous coronary intervention 经皮冠状动脉介入干预Pco2 carbon dio*ide partial pressure 二氧化碳分压力Pco2 carbon dio*ide partial tension 二氧化碳分力PCR polymerase chain reaction 聚合酶链反响PCV packed cell volume 血细胞压积PCWP pulmonary capillary wedge pressure 肺毛细血管楔压PDA patent ductus arteriosus 动脉导管未闭PDA posterior descending coronary artery 冠脉后降支PDE phosphodiesterase 磷酸二酯酶PDIs Phosphodiesterase inhibitors 磷酸二酯酶抑制剂PDGF platelet derived growth factor 血小板源生长因子PEA pulseless electrical activity 无脉性电活动PEEP positive ende*piratory pressure 呼气末正压呼吸PES programmed electrical stimulation 程控电刺激PET positron emission-puted tomography 正电子发射型计算机断层显像PF4 platelet factor 4 血小板第4因子PG prostaglandin 前列腺素PGI2 prostacyclin 前列环素PICVI Percutaneous in situ coronary venous arterialization 经皮原位冠状静脉动脉化PJRT permanent junctional repciprocating tachycardia 持久性交界性交互心动过速PJT paro*ysmal junctional tachycardia 阵发性交界性心动过速PKC protein kinase C 蛋白激酶CPLAATO Percutaneous Left Atrial Appendage Transcatheter Occluder 经皮导管左心耳闭塞器PLS prolonged life support 延续生命支持PMI point of ma*imal impulse 最强心尖搏动点PMVL posterior mitral valve leaflet 二尖瓣后叶PMT pacemaker mediated tachycardia 起搏器介入性心动过速PO2 o*ygen partial pressure 氧分压力PO2 o*ygen partial tension 氧分力POCT point of care test 床旁检查PPAR pero*isome proliferator-activated receptor 过氧化物酶体增生物活化受体PPD purified protein derivative (tuberculin) 精制蛋白衍化物〔结核菌素〕PR peripheral resistance 外周阻力PR pulmonic regurgitation 肺动脉瓣关闭不全PRA plasma renin activity 血浆肾素活性PRG phleborheography 静脉血流描记法PS protein S 蛋白SPS pulmonic stenosis 肺动脉瓣狭窄PS pulmonary stenosis 肺动脉瓣狭窄PSM presystolic murmur 收缩前杂音PSVT paro*ysmal supraventricular tachycardia 阵发性室上性心动过速PT prothrombin time 凝血酶原时间PT pulmonary trunk 肺动脉干PTA plasma thromboplastin 血浆凝血致活酶前质PTC plasma thromboplastin ponent 血浆凝血致活酶成分PTCA percutaneous transluminal coronary angioplasty 经皮冠状动脉血管成形术Ptf P- wave terminal force 心房终末电压PTT partial thromboplastin time 局部凝血活酶时间PUO pyre*ia of unknown origin 原因不明的发热,无名热PVCs premature ventricular contractions 室性早搏PVE prosthetic valve endocarditis 人工瓣膜性心膜炎PVR pulmonary vascular resistance 肺血管阻力PVT polymorphic ventricular tachycardia 多形性室性心动过速PWT posterior wall thickness 后壁厚度QQMI Q_wave myocardial infarction Q波型心肌堵塞QTd Q-T dispersion Q-T离散度QTc corrected QT interval 校正的QT间期RRA right arm 右臂RA right atrium 右心房RAD right a*is deviation 电轴右偏RAAS renin-angiotensin-aldosterone system 肾素-血管紧素-醛固酮系统RAE right atrial enlargement 右心房扩大RAO right anterior oblique 右前斜位RAS renin-angiotensin system 肾素-血管紧素系统RBBB right bundle branch block 右束支传导阻滞RBC red blood cell 红细胞RBC red blood (cell) count 红细胞计数RCA right coronary artery 右冠状动脉RCM restrictive cardiomyopathy 限制性心肌病RCTs randomized controlled trials 随机对照研究RES reticuloendothelial system 网状皮系统RF rheumatoid factor 类风湿因子RFCA radiofrequency catheter ablation 射频消融术RFLP restriction fragment length polymorphism 限制性片段长度多态性PHC Right-sided heart catheterization 右心导管检查RIST radioimmunosorbent test 放射免疫吸附试验RKY roentgenkymography *线记波照相术RNA ribonucleic acid 核糖核酸RNP ribonucleoprotein 核糖核酸蛋白ROM passive range of motion 被动活动ROSC return of spontaneous circulation 自主循环恢复RPF renal plasma flow 肾血浆流量RPS renal pressor substance 肾加压物质RQ respiratory quotient 呼吸商rT3 reverse triiodothyronine 反三碘甲状腺原氨酸r-TPA rebinant tissue plasminogen activator 重组的组织型纤溶酶原激活物RV residual capacity 残气量RV right ventricle 右心室RVAD right ventricular assist device 右心室辅助装置RVH right ventricular hypertrophy 右心室肥大RVI right ventricle infarction 右心室堵塞RVOT right ventricular outflow Tract 右室流出道SS1 first heart sound 第一心音S2 second heart sound 第二心音S3 third heart sound 第三心音S4 fourth heart sound 第四心音SA sinoatrial 窦房的SACT sinoatrial conduction time 窦房传导时间SAB sinoatrial block 窦房阻滞SAECG signal averaged electrocardiogram 信号叠加心电图SAH systemic arterial hypertension 体循环动脉高压SAH subarachnoid hemorrhage 蛛网膜下腔出血SAM systolic anterior motion 〔二尖瓣前叶〕在收缩期前移SB sinus bradycardia 窦性心动过缓SBE subacute bacterial endocarditis 亚急性细菌性心膜炎SBP systolic blood pressure 收缩压SBT serum bactericidal titer 血清杀菌剂滴度SC closure of the semilunar valves 半月瓣关闭SC subcutaneous 皮下SCD sudden cardiac death 心脏性猝死scu-PA single chain urokinase-type plasminogen activator 单链尿激酶型纤溶酶原激活物SD standard deviation 标准差SE stress echocardiography 负荷超声心动图SE standard error 标准误差SEC spontaneous echo contrast 自发性声学显影SFMC soluble fibrin monomer ple* 可溶性纤维蛋白单体复合物SGOT glutamic o*aloacetic acid transferase 血清谷草转氨酶SH sulfhydryl 巯基SHR spontaneously hypertensive rat 自发性高血压大鼠SHRSP strok-prone SHR 具有中风倾向的自发性高血压大鼠SIRS systemic inflammatory response syndrome 全身炎症反响综合征SK streptokinase 链激酶SL sublingual 舌下SLE systemic lupus erythematosus 系统性红斑狼疮SM systolic murmur 收缩期杂音SMBG self-monitoring blood glucose 自我监测血糖SMCS smooth muscle cells 平滑肌细胞SMI silent myocardial ischemia 无病症性心肌缺血SNRT sinus node recovery time 窦房结恢复时间SNS sympathetic nervous system 交感神经系统SOB shortness of breath 呼吸短促SPECT single photon emission puted tomography 单光子发射型计算机断层显像SQTS short Q-T syndrome 短Q-T 间期综合征SR sarcoplasmic reticulum 肌浆质网ssDNA single-stranded DNA 单链DNASSS sick sinus syndrome 病态窦房结综合症ST sinus tachycardia 窦性心动过速STI systolic time intervals 心室收缩时间间期SUDS sudden une*plained death syndrome 不明原因猝死综合症SUNDS sudden une*plained nocturnal death syndrome 不明原因的夜间猝死综合症SV stroke volume 每搏心输出量SVC superior vena cava 上腔静脉SVI stroke volume inde* 每搏量指数SVT supraventricular tachycardia 室上性心动过速SWI stroke work inde* 每搏作功指数TTa atrial repolarization 心房复极TABD triple acid-base disorders 三重性酸碱失衡TAT thrombin -antithrombin ple* 凝血酶-抗凝血酶复合物TC total cholesterol 总胆固醇Tc technetium 锝TDI tissue doppler imaging 组织多普勒成像TDP torsades de pointes 尖端扭转性室性心动过速TEE transesophageal echocardiography 经食道超声心动图TET treadmill e*ercise test 踏车运动试验TFPI tissue factor pathway inhibitor 组织因子途径抑制物TGA transposition of the great arteries 大动脉转位TGB thyro*ine-binding globulin 甲状腺素结合球蛋白TGF-β transforming growth factor-beta 转化生长因子βTHAM tromethamine 三羟甲基氨基甲烷TIA transient ischemic attack 短暂性脑缺血发作TIMI thrombolysis in myocardial infarction 心肌堵塞溶栓TLC total lung capacity 肺总量TM thrombomodulin 血栓调节蛋白TMLR transmyocardial laser revascularization 心肌再血管化TMST treadmill e*ercise test 踏车运动试验TNF tumor necrosis factor 肿瘤坏死因子T-PA tissue-type plasminogen activator 组织型纤溶酶原激活物TPP thrombus precussor protein 血栓前体蛋白TR tricuspid regurgitation 三尖瓣返流TRH thyrotropin-releasing hormone 促甲状腺素释放激素TS tricuspid stenosis 三尖瓣狭窄TSH thyroid-stimulating hormone 促甲状腺素TT thrombin time 凝血酶时间TT thrombolytic therapy 溶栓治疗TTE transthoracic echocardiography 经胸超声心动图TV tricuspid valve 三尖瓣T*A2 thrombo*ane A2 血栓烷A2T*B2 thrombo*ane B2 血栓烷B2UUA unstable angina 不稳定性心绞痛UCG ultrasound cardiogram 超声心动图UCM unclassified cardiomyopathies 不定型的心肌病UK urokinase 尿激酶u-PA urokinase type plasminogen activator 尿激酶型纤溶酶原激活物URL upper rate limit 上限频率URTI upper respiratory tract infection 上呼吸道感染US ultrasound 超声VV4R right precordial lead in V4 position 右胸导联V4的位置VAD ventricular assist device 心室辅助装置VC vital capacity 肺活量VCAM vascular cell adhesion molecule 血管细胞粘附分子VCG vectorcardiogram 心电向量图Vco2 carbon dio*ide 二氧化碳产量VDH valvular disease of the heart 心瓣膜病VE minute ventilation 每分钟通气量VEDP ventricular end-diastolic pressure 心室舒末压力VEGF vascular endothelial growth factor 血管皮细胞生长因子VF ventricular fibrillation 室颤VFT ventricular fibrillation threshold 室颤阈值VLDL very-low-density lipoprotein 极低密度脂蛋白VLP ventricular late potential 心室晚电位VMA vanillylmandelic acid 香草扁桃酸Vo2 peak o*ygen consumption 峰值氧耗Vo2 respiratory o*ygen uptake 呼吸摄氧量VMA vanillylmandelic acid 3-甲氧基-4羟基苦杏仁酸VPBs ventricular premature beats 室性早搏VPC ventricular premature ple* 心室早搏复合波VPD ventricular premature depolarization 心室过早去极化VRP ventricular refractory period 心室不应期VSD ventricular septal defect 室间隔缺损VT ventricular tachycardia 室性心动过速VTE venous thromboembolism 静脉血栓栓塞VW vessel wall 血管壁vWF von willebrand factor 血管性血友病因子WWBC white blood cell 白细胞WBC white blood (cell) count 白细胞计数WHO world health organization 世界卫生组织α-MHC alpha-myosin heavy chain α-肌凝蛋白重链β-TG β-th romboglobulin β-血小板球蛋白23-DPG 23-diphosphoglycerate 23-二磷酸甘油酸5-HT 5-hydro*ytryptamine 5-羟色胺123I MIBG iodine-123 metaiodobenzylguanidine I123标记的间碘苄胍17-KS 17-ketosteroids 17-酮皮质类固醇17-OHCS 17-hydro*ycorticosteroid 17-羟皮质类固醇18-OHD 18-hydro*ycorticosterone 18-羟皮质酮24hUFC 24h urine free cortisol 24小时尿液游离皮质醇。

IChO国际化学奥林匹克竞赛考试大纲

IChO国际化学奥林匹克竞赛考试大纲

SYLLABUS OF THEINTERNATIONAL CHEMISTRY OLYMPIADPart I Theoretical partLevel 1: These topics are included in the overwhelming majority of secondary school chemistry programs and need not be mentioned in the preparatory problems.Level 2: These topics are included in a substantial number of secondary school programs and maybe used without exemplification in the preparatory problems. Level 3: These topics are not included in the majority of secondary school programs and can only be used in the competition if examples are given in the preparatory problems.1.The atom1.1.Introduction1.1.1.Counting of nucleons 11.1.2.Isotopes 1 1.2.The hydrogen atom1.2.1.Concept of energy levels 11.2.2.Shape of s-orbitals 11.2.3.Shape and orientation of p-orbitals 11.2.4.Shape and orientation of d -orbitals 31.2.5.Understanding the simplest Schrodinger equation 31.2.6.Square of the wave function and probability 31.2.7.Quantum numbers (n, l, m l) 3 1.3.Radioactivity1.3.1.Types of radioactivity 11.3.2.Radioactive decay 11.3.3.Nuclear reactions 22.Chemical bonding2.1.VSEPR - Simple molecular structures with2.1.1.no more than four electron pairs about central atom 12.1.2.with central atom exceeding the “octet rule”3 2.2.Delocalization and resonance3 2.3.Hybrid orbital theory3 2.4.Molecular orbital theory2.4.1.molecular orbital diagram (H2 molecule) 32.4.2.molecular orbital diagram (N2 and O2 molecules) 32.4.3.bond orders in O2, O2-, O2+ 32.4.4.unpaired electrons and paramagnetism 33.Chemical calculations3.1.1.Balancing equations 13.1.2.Stoichiometric calculations 13.1.3.Mass and volume relations (including density) 13.1.4.Empirical formula 13.1.5.Avogadro’s number 13.1.6.Concentration calculations 14.Periodic trends4.1.Electron configuration 4.1.1. Pauli exclusion principle14.1.2.Hund’s Rule 14.1.3.Main group elements 14.1.4.Transition metal elements 14.1.nthanide and actinide metals 3 4.2.Electronegativity 1 4.3.Electron affinity 2 4.4.First ionization energy 1 4.5.Atomic size 1 4.6.Ion size 14.7.Highest oxidation number 15.Inorganic Chemistry5.1.Introduction5.1.2.Trends in physical properties of elements (Main groups)5.1.2.1.melting point 15.1.2.2.boiling point 15.1.2.3.metal character 15.1.2.4.magnetic properties 35.1.2.5.electrical conductivity 25.1.3.Oxidation number 15.1.4.Nomenclature 5.1.3.1. main group compounds15.1.4.1.transition metal compounds 15.1.4.2.simple metal complexes 3 5.2.Groups 1 and 2 5.2.1. Trend in reactivity of (heavy elements more reactive) 15.2.2.Products of reaction with 5.2.2.1. water15.2.2.1.halogens 15.2.2.2.oxygen 25.2.3.Basicity of oxides 15.2.4.Properties of hydrides 35.2.5.Other compounds, properties and oxidation states 3 5.3.Groups 13 - 18 and Hydrogen5.3.2.Binary molecular compounds of hydrogen 5.3.1.1. Formulae 15.3.2.1.Acid-base properties of CH4, NH3, H2O, H2S 15.3.2.2.Other properties 35.3.3.P block elementsGroup 13 (Boron group) 5.3.2.1 The oxidation state of boron andaluminium in their 1 oxides and chlorides is +35.3.3.1.The acid-base properties of aluminium 2oxide/hydroxide5.3.3.2.Reaction of boron(III) oxide with water 35.3.3.3.Reaction of boron(III) chloride with water 35.3.3.4.Other compounds, properties and oxidation states 35.3.4.Group 14 (Carbon group)5.3.4.1.The oxidation state of Si in its chloride and oxide is 1 +45.3.4.2.The +2 and +4 oxidation states of carbon, tin and 2 lead, theacid-base and redox properties of the oxides and chlorides5.3.4.3.Other compounds, properties and oxidation states 35.3.5.Group 15 (Nitrogen group)5.3.5.1.Phosphorus(+5) oxide and chloride, and their 2 reaction withwater5.3.5.2.Phosphorus(+3) oxide and chloride, and their 2 reaction withwater5.3.5.3.Oxides of nitrogen a. Reaction of NO to form NO2 1b.Dimerization of NO2 1c.Reaction of NO2 with water 15.3.5.4.Redox properties of a. HNO3 and nitrates 1b. HNO2 and NH2NH2 35.3.5.5.Bi(+5) and Bi( + 3) 35.3.5.6.Other compounds, properties and oxidation states 35.3.6.Group 16 (Oxygen group)5.3.6.1.The +4 and +6 oxidation states of sulfur, reaction 1 of theiroxides with water, properties of their acids5.3.6.2.Reaction of thiosulfate anion with I2 35.3.6.3.Other compounds, properties and oxidation states 35.3.7.Group 17 (Halogens)5.3.7.1.Reactivity and oxidant strength decreases from F2 1to I25.3.7.2.Acid-base properties of the hydrogen halides 15.3.7.3.The oxidation state of fluorine in its compounds is 1 -15.3.7.4.The -1, +1, +3, +5, +7 oxidation states of chlorine 15.3.7.5.Mononuclear oxoanions of chlorine 25.3.7.6.Reactions of halogens with water 35.3.7.7.Reaction of Cl2O and CI2O7 with water 35.3.7.8.Other compounds, properties and oxidation states 35.3.8.Group 18 (Rare gases) 3 5.4.Transition elementsmon oxidation states of common transition metals: 1Cr(+2), Cr(+3) Mn(+2), Mn(+4), Mn(+7) Ag(+1) Fe(+2), Fe(+3)Co(+2) Zn(+2) Hg(+1), Hg(+2) Cu(+1), Cu(+2) Ni(+2)5.4.3.Colours of ions listed above in aqueous solution 25.4.4.Insolubility of Ag, Hg and Cu in HCl 25.4.5.M2+ arising by dissolution of the other metals in HCl 25.4.6.Cr(OH)3 and Zn(OH)2 are amphoteric and the other +2 2oxides/hydroxides of the metals listed above are basic5.4.7.MnO4- and Cr2O72- are strong oxidants in acid solution 15.4.8.pH dependence of products of MnO4- acting as oxidant 25.4.9.Interconversion between CrO42- and Cr2O72- 35.4.10.Other compounds, properties and oxidation states 3 nthanides and actinides3 5.6.Coordination chemistry including stereochemistry5.6.2.Definition of coordination number 15.6.3.Writing equations for complexation reactions given all 1formulae5.6.4.Formulae of common complex ions5.6.4.1.Ag(NH3)2+ 15.6.4.2.Ag(S2O3)23- 35.6.4.3.FeSCN2+ 35.6.4.4.Cu(NH3)42+ 15.6.4.5.Other complex ions 35.6.5.(6.5) Ligand field theory (e g and 12g terms, high and low spin) 35.6.6.Stereochemistry5.6.6.1.(6.7) cis and trans35.6.6.2.enantiomers 3 5.7.Selected industrial processes5.7.2.Preparation of H2SO4 15.7.3.PreparationofNH3 15.7.4.PreparationofNa2cO3 25.7.5.PreparationofCl2 and NaOH 25.7.6.PreparationofHNO3 26.Physical chemistry6.1.Gases6.1.2.Ideal gas law 16.1.3.van der Waal’s gas law36.1.4.definition of partial pressure 26.1.5.Dalton’s Law3 6.2.Thermodynamics6.2.2.First Law6.2.2.1.Concept of system and surroundings 26.2.2.2.Energy, heat and work 26.2.3.Enthalpy6.2.3.1.Relationship between internal energy and enthalpy 36.2.3.2.Definition of heat capacity 26.2.3.3.Difference between C p and C v (ideal gas only) 36.2.3.4.Enthalpy is a state property (Hess’s Law) 26.2.3.5.Born-Haber cycle for ionic compounds 3e of standard formation enthalpies 26.2.3.7.Enthalpies of solution and solvation 36.2.3.8.Bond enthalpies (definition and use) 26.2.4.Second Law (Entropy and Free Energy)6.2.4.1.Entropy definition (dq / T)36.2.4.2.Entropy and disorder 36.2.4.3.Entropy definition (S = k ln W) 36.2.4.4.Gibbs energy definition (A G = A H - T A S) 3ing A G to predict direction of natural change 36.2.4.6.Relationship between A G° and equilibrium constant K3 6.3.Equilibrium6.3.2.Acid-base6.3.2.1.Arrhenius definitions of acids and bases 16.3.2.2.Bronsted-Lowry definitions 16.3.2.3.Conjugate acids and bases 16.3.2.4.pH definition 16.3.2.5.K w definition 16.3.2.6.K a and K b as a measure of acid and base strength 16.3.2.7.Acidity or basicity of ions 16.3.2.8.Calculation of pH from p K (weak acid) 1a6.3.2.9.Calculation of pH of a simple buffer solution 26.3.3.Gas phase6.3.3.1.Equilibrium constant in partial pressures 36.3.3.2.Relating K and K c 36.3.4.Solubility P6.3.4.1.Solubility constant (product) definition (K s p) 26.3.4.2.Calculation of solubility in water from K 2s sppleximetricplex formation constant (definition) 36.3.5.2.Problems involving compleximetric equilibria 36.3.5.3.Lewis acids and bases 36.3.5.4.Hard and soft Lewis acids and bases 36.3.6.Phase6.3.6.1.Temperature dependence of vapour pressure 36.3.6.2.Clausius-Clapeyron equation 36.3.6.3.Single component phase diagramsa.triple point 3b.critical point 36.3.6.4.liquid-vapour systema.ideal and nonideal systems 3b.diagram 3e in fractional distillation 36.3.6.5.Henry’s Law36.3.6.6.Raoult’s Law36.3.6.7.Deviation from Raoult,s Law 36.3.6.8.Boiling point elevation 36.3.6.9.Freezing point depression 36.3.6.10.Osmotic pressure 36.3.6.11.Partition coefficient 36.3.6.12.Solvent extraction 36.3.7.Multiple6.3.7.1.Calculation of pH for multiprotic acids 36.3.7.2.Calculation of pH for weak acidmixtures 3 6.4.Electrochemistry6.4.2.Electromotive force (definition) 16.4.3.First kind electrodes 16.4.4.Standard electrode potential 16.4.5.Nernst equation 36.4.6.Second kind electrodes 36.4.7.Relationship between G and electromotive force 37.Chemical kinetics (Homogeneous reactions)7.1.Introduction7.1.2.Factors affecting reaction rate 17.1.3.Reaction coordinates and thebasic idea of a transition state 17.2.Rate law7.2.2.Differential rate law 27.2.3.Concept of reaction order 27.2.4.Rate constant definition 27.2.5.First order reactions7.2.5.1.Dependence of concentration on time 37.2.5.2.Concept of half life 37.2.5.3.Relationship between half life and rate constant 37.2.5.4.Calculation of first order rate constant from a. differential rate law 3b. integrated rate law 37.2.5.5.Rate constant for second and third order reactions 3 7.3.Reaction mechanisms7.3.2.Concept of molecularity 37.3.3.Rate-determining step 37.3.4.Basic concepts of collision theory 37.3.5.Opposing parallel and consecutive reactions 37.3.6.Arrhenius’s law37.3.6.1.Definition of activation energy 37.3.6.2.Calculation of activation energy 38.Spectroscopy8.1.UV/visible8.1.2.Identification of aromatic compound 38.1.3.Identification of chromophore 38.1.4.Dyes: colour vs structure 38.1.5.Beer’s Law3 8.2.Infrared8.2.2.Interpretation using a table of frequencies 38.2.3.Recognition of hydrogen bonds 3 8.3.x-Ray8.3.2.Bragg,s Law 38.3.3.Concept of8.3.3.1.coordination number 38.3.3.2.unit cell 38.3.4.Solid structures8.3.4.1.NaCl 38.3.4.2.CsCl 38.3.4.3.metals 38.4.1.General Concepts 8.4.1.1. chemical shift38.4.1.2.spin-spin coupling and coupling constants 38.4.1.3.integration 38.4.2.Interpretation of a simple 1H spectrum (like ethanol) 38.4.3.Identification of o- and p-disubstituted benzene 38.4.4.Interpretation of simple spectra of 13C (proton decoupled) and 3other 1/2 spin nuclei8.5. Mass spectrometry8.5.1.1.Recognition of molecular ion 38.5.1.2.Recognition of fragments with the help of a table 38.5.1.3.Recognition of typical isotope distribution 3anic Chemistry9.1.Introduction 9.1.1. (3.1.1) Alkane naming (IUPAC) 19.1.2.Trends in boiling points of9.1.2.1.(3.1.3) alkanes with structure 19.1.2.2.(3.7.1) alcohols vs ethers due to hydrogen-bonding 19.1.3.(3.3.1, 3.4.1) Geometry at singly, doubly, and triply bonded 1 carbon9.1.4.Identification of common functional groups 19.1.5.Isomerism of alkenes 9.1.5.1. cis - trans19.1.5.1.E/ Z39.1.6.Enantiomers9.1.6.1.Optical activity 29.1.6.2.R/S nomenclature 3 9.2.Reactivity9.2.2.Alkanes9.2.2.1.reaction with halogens a. products 1b. free radical mechanism (initiation,termination) 29.2.2.2.Cycloalkanes a. names 2b.Strain in small rings 3c.chair/boat conformations of cyclohexane 39.2.3.Alkenes9.2.3.1.Products from Br2, HBr and H2O/H+ 19.2.3.2.Markownikoff’s rule 29.2.3.3.Mechanism involving carbocation intermediates 39.2.3.4.Relative stability of carbocations 39.2.3.5.1,4 addition to dienes 39.2.4.Alkynes 9.2.3.1. Acidity relative to alkenes39.2.4.1.Differences in chemical properties from alkenes 29.2.5.Benzene 9.2.4.1. formula19.2.5.1.stabilization by resonance 19.2.5.2.electrophilic substitution (nitration, halogenation)a.directing effect of first substituent 3b.effect of first substituent on reactivity 3c.explanation of substituent effects 39.2.6.Halogen compounds 9.2.5.1. Nomenclature of monofunctional19.2.6.1.Substitution reactionsa.giving alcohols 3b.in which halogen is exchanged 3c.reactivityi.primary i/s secondary i/s tertiary 3ii.aliphatic /s aromatic 3d.S N1 and S N2 mechanisms 39.2.6.2.Elimination reactions 2petition of elimination and substitution 2 9.2.7.Alcohols 9.2.6.1. Nomenclature of monofunctional1parison of acidity of alcohols and phenols 29.2.7.2.Dehydration to alkenes 19.2.7.3.Esters with inorganic acid 29.2.7.4.Oxidation reactions 1 9.2.8.Aldehydes and ketones 9.2.7.1. Nomenclature of monofunctional19.2.8.1.Oxidation of aldehydes 19.2.8.2.Reduction to alcohols (LiAlH4, NaBH4) 39.2.8.3.Keto/enol tautomerism 39.2.8.4.Nucleophilic addition reactions witha.HCN 3b.RNH2 (R = alkyl, HO, NH2) 3c.enolate anions (aldol condensation) 3d.alcohols to form acetals/ketals 3e.Grignard reagents 39.2.9.Carboxylic acids and their derivatives 9.2.8.1.Nomenclature of carboxylicacids and their 2 derivatives (esters, acid halides, amides)9.2.9.1.Acidity strength related to inductive effects 39.2.9.2.Preparation of carboxylic acids by hydrolysis of a. esters(including soaps) 1b.amides 2c.nitriles 39.2.9.3.Reaction of carboxylic acids a. with alcohols to form esters 1b.to form acid chlorides 3c.to form anhydrides 39.2.9.4.Reaction of acid chlorides to form amides 39.2.9.5.Mechanism of esterification 39.2.9.6.Multifunctional acids (hydroxyacids, ketoacids) 39.2.9.7.Polycarboxylic acids 39.2.10.Amines9.2.10.1.Nomenclaturea.simple amines 1b.recognition of primary, secondary, tertiary 19.2.10.2.Basicitya.As a property of an amine 1parison of basicity of aliphatic and aromatic 3parison of basicity of amines and amides 3d.Preparation of aminesi.from halides 3ii.from aromatic nitro compounds 3iii.from amides (by hydrolysis) 39.2.10.3.Diazotizationa.of aliphatic amines 3b.of aromatic amines 310.Polymers10.1.Synthetic10.1.2.Addition polymers10.1.2.1.polystyrene 210.1.2.2.polyethene 110.1.2.3.chain mechanism of formation 210.1.3.Condensation polymers10.1.3.1.polyesters 210.1.3.2.polyamides 210.1.4.Silicones 310.1.5.Concept of cross-linking and its affect on properties 3 10.2.. Natural10.2.2.Silicates10.2.3.Rubber11.Biochemistry11.1.Carbohydrates11.1.2.Glucose and fructose11.1.2.1.chain formulae 111.1.2.2.Fischer projections 211.1.2.3.Haworth formulae 311.1.3.Difference between starch and cellulose 211.1.4.Difference between a- and p- D glucose 2 11.2.Fats11.2.2.Structure of fats in relationship to properties 211.2.3.Formula of glycerol 1 11.3.Nitrogen-containing Compounds of Biological Importance11.3.2.Amino acids 11.3.1.1. Ionic structure111.3.2.1.Isoelectric point 311.3.2.2.20 amino acids (classification with structures 2provided)11.3.2.3.Separation by electrophoresis 311.3.2.4.The peptide linkage 111.3.3.Proteins11.3.3.1.Primary structure 111.3.3.2.-S-S- bridges 311.3.3.3.Sequence analysis 311.3.3.4.Secondary structure 311.3.3.5.Details of a-helix structure 311.3.3.6.Tertiary structure 311.3.3.7.Denaturation (change inpH, temperature, 2metals, ethanol)11.3.4.Nuclei Acids and Protein Synthesis11.3.4.1.Pyrimidine and purine 311.3.4.2.Nucleosides and nucleotides 311.3.4.3.Formulae of pyrimidine and purine bases 311.3.4.4.Difference between ribose and 2-deoxyribose 311.3.4.5.Base combination CG and AT (hydrogen-bonding) 311.3.4.6.Difference between DNA and RNA 311.3.4.7.Difference between mRNA and tRNA 3 11.4.Enzymes11.4.2.1.General properties, active centers 311.4.2.2.Nomenclature, kinetics, coenzymes, function of ATP 312.Analytical chemistry12.1.Titrations12.1.2.acid-base12.1.2.1.Titration curve; pH (strong and weak acid) 212.1.2.2.Choice of indicators for acidimetry 212.1.3.Redox titration 312.2.Qualitative analysis12.2.2.Ions (Inorganic)12.2.2.1.Identification of Ag+, Ba z+, Cl-, SO42- 212.2.2.2.Identification of other anions and cations 3anic functional groups12.2.3.1.Lucas reagent (1-, 2-, 3-alcohols) 312.2.3.2.Iodoform reaction 312.2.3.3.Identification of primary, secondary, tertiary, 3quarternary amines in the laboratory12.3.Chromatographic methods of separation 3Part I Experimental partLevel 1: is assigned to the basic experimental activities which are supposed to be mastered by competitors very wellLevel 2: is assigned to the activities which are parts of school experimental exercises in developed countries and the authors of IChO tasks may incorporate them into the tasks without beingbounded to mention it in advanceLevel 3: is assigned to such activities which are not in the chemistry syllabus in the majority of participating countries and the authors are obliged to mention them in the set of preparatorytasksIf the organizer wants to apply a technique which is not mentioned in the above syllabus, this technique is set to level 3 automatically.1.Synthesis of inorganic and organic compounds1.1.Heating with burners and hotplates 1 1.2.Heating of liquids 1 1.3.Handling the work with inflammable substances and materials 1 1.4.Measuring of masses (analytical balance) 1 1.5.Measuring of volumes of liquids (measuring cylinder, pipette, 1burette)1.6.Preparation of solutions from a solid compound and solvent 1 1.7.Mixing and dilution of solutions 1 1.8.Mixing and stirring of liquids 1 ing mixer and magnetic stirrer 2 ing a dropping funnel 1 1.11.Syntheses in flat bottom vessels - general principles 1 1.12.Syntheses in round bottom vessels - general principles 1 1.13.Syntheses in a closed apparatus - general principles 1 1.1ing microscale equipment for synthesis 3 1.15.Apparatus for heating of reaction mixture under reflux 2 1.16.Apparatus for distillation of liquids at normal pressure 21.17.Apparatus for distillation of liquids at reduced pressure 2 1.18.Apparatus for steam distillation 3 1.19.Filtration through flat paper filter 1 1.20.Filtration through a folded paper filter 1 1.21.Handling a water vacuum pump 1 1.22.Filtration through a Buchner funnel 1 1.23.Suction through a glass filter 1 1.24.Washing of precipitates by decantation 1 1.25.Washing of precipitates on a filter 2 1.26.Drying of precipitates on a filter with appropriate solvents 2 1.27.Recrystallization of substances from aqueous solution 1 1.28.Recrystallization of substances from a known organic solvent 2 1.29.Practical choice of an appropriate solvent for recrystallization of a 3substance1.30.Drying of substances in a drying box 2 1.31.Drying of substances in a desiccator 2 1.32.Connecting and using of a gas washing bottle 21.33.Extraction with an inmiscible solvent 12.Identification of inorganic and organic compounds:general principles2.1.Test-tube reactions 1 2.2.Technique of reactions performed in a dot dish and on a filter paper 12.3.Group reactions of some cations and anions specified by the 2organizer2.4.Selective reactions of some cations and anions specified by the 2 organizer2.5.Specific reactions of some cations and anions specified by the organizer 3 2.6.Identification of elements by flame coloration (using a platinum 2wire/MgO rod, Co-glass)ing a hand spectroscope/Bunsen spectroscope 3 2.8.Melting point determination with Kofler or similar type of apparatus 3 2.9.Qualitative evidence of basic functional groups of organic 2substances specified by the organizer2.10.Exploitation of some specific reactions for identification of organic 3compounds (specified by the organizer)3.Determination of some inorganic and organic compounds:general principles3.1.Quantitative determinations using precipitation reactions 2 3.2.Igniting of a precipitate in a crucible 1 3.3.Quantitative volumetric determinations 1 3.4.Rules at titrating 1e of a pipetting ball 1 3.6.Preparation of a standard solution 2 3.7.Alkalimetric and acidimetric determinations 2 3.8.Color transitions of indicators at alkalimetric and acidimetric 2determinations3.9.Direct and indirect determinations (back titration) 3 3.10.Manganometric determinations 3 3.11.Iodometric determinations 3 3.12.Other types of determinations on basis of redox reactions 3 plexometric determinations 3 3.14.Color transitions of solutions at complexometric determinations 3 3.15.Volumetric determinations on basis of precipitation reactions 33.16.Thermometric titration 34.Special measurements and procedures4.1.Measuring with a pH-meter 2 4.2.Chromatography on thin layers 3 4.3.Column chromatography 3 4.4.Separation on ion exchanger 3 4.5.Measuring of UV-VIS absorbances with a spectral photometer 34.6.Performing of conductivity measurements 35.Evaluation of results5.1.Estimation of experimental errors (significant figures, plots scales) 1。

SIMV联合PSV通气方案在急诊老年Ⅱ型呼吸衰竭患者抢救中的应用研究

SIMV联合PSV通气方案在急诊老年Ⅱ型呼吸衰竭患者抢救中的应用研究

SIMV联合PSV通气方案在急诊老年Ⅱ型呼吸衰竭患者抢救中的应用研究作者:谢冬冰来源:《中国现代医生》2022年第11期[摘要] 目的探討SIMV联合PSV通气方案在急诊老年Ⅱ型呼吸衰竭患者抢救中的临床治疗效果。

方法选择2018年2月至2020年2月福州市第一医院收治的100例老年Ⅱ型呼吸衰竭患者进行本次研究,抽签法将患者分为研究组(n=50)和对照组(n=50)。

对照组采用同步间歇指令通气(SIMV)治疗,研究组采用SIMV联合压力支持通气(PSV)治疗。

比较两组的撤机时间、ICU住院时间、撤机成功率,对比治疗前后呼吸力学,动脉血气,血清C-反应蛋白(CRP)、降钙素原(PCT)、白细胞介素-6(IL-6)水平。

结果治疗后,研究组撤机时间、ICU住院时间均显著短于对照组,撤机成功率显著高于对照组,差异有统计学意义(P[关键词] 同步间歇指令通气;压力支持通气;呼吸衰竭;呼吸力学;动脉血气[中图分类号] R563.8 [文献标识码] B [文章编号] 1673-9701(2022)11-0045-03[Abstract] Objective To explore the clinical effect of synchronous intermittent mandatory ventilation(SIMV) combined with pressure support ventilation (PSV) in the rescue of elderly patients with type 2 respiratory failure (T2RF). Methods A total of 100 elderly patients with T2RF treated in the First Hospital of Fuzhou from February 2018 to February 2020 were selected for this study. They were divided into the study group (n=50) and the control group (n=50) according to the method of drawing lots. The control group was treated with synchronous intermittent mandatory ventilation (SIMV), while the study group was treated with SIMV combined with PSV. The weaning time, ICU stay time and weaning success rate of two groups were compared, and the respiratory mechanics, arterial blood gas, serum C-reactive protein (CRP), procalcitonin (PCT) and interleukin-6(IL-6) levels before and after treatment were compared between the two groups. Results After treatment, the weaning time and ICU stay time in the study group were significantly shorter than those in the control group, and the weaning success rate in the study group was significantly higher than that in the control group, with statistically significant difference (P[Key words] Synchronous intermittent mandatory ventilation; Pressure support ventilation; Respiratory failure; Respiratory mechanics; Arterial blood gas急诊老年Ⅱ型呼吸衰竭,又名高碳酸性呼吸衰竭,由于各种原因导致患者肺通气和(或)换气功能出现严重障碍,从而无法进行气体交换,出现呼吸困难、心率加快等常见的临床症状。

英文名词解释

英文名词解释

Introduction of Pathophysiology1.PathophysiologyPathophysiology is a science to study on the mechanisms and laws of occurrence and development of diseases.Conspectus of Disease1.DiseaseDisease is referred as an aberrant manifestation of homeostatic disturbances caused by harmful agents.2.Causative factor / pathogenic causeCausative factor or pathogenic cause is referred as the factor that can cause a disease and determine its specificity.3.Alternation of the cause and effectAlternation of the cause and effect means that during the development of a disease, the original cause can result in certain changes of the body and these changes can in turn lead to another alternations under some conditions. That is to say, the original pathogenic factor of a disease leads to a result and the latter can be transformed into the cause of further alternations under certain conditions. In this way, the successive alternation and transformation of cause and effect promote the progression of the disease.4.Vicious cycleVicious cycle is a circular process of the alternate cause-effect, in which every alternation of cause and effect will bring about more serious injuries to the body and further spoil the health condition. The final result of this kind of alternative circulation is to cause the patient to die.5.Brain deathBrain death is a state of permanent irreversible cessation of whole brain activity. At that time, the function of the patient's body as a whole body has stopped forever.Water and Sodium Balance and Imbalance1.Hypovolemic hyponatremiaHypovolemic hyponatremia is hyponatremia with decreased extracellular fluid volume. In this situation, sodium loss is more than water loss, and serum sodium concentration falls below 130mmol/L and plasma osmotic pressure is less than 280mmol/L. It is also termed hypotonic dehydration or hypo-osmotic dehydration.2.Hypovolemic hypernatremiaHypovolemic hypernatremia is hypernatremia with decreased extracellular fluid volume. In this situation, water loss is more than sodium loss, serum sodium concentration is more than 150mmol/L, and plasma osmotic pressure is more than 310mmol/L. It is also termed hypertonic dehydration or hyperosmotic dehydration.3.Isotonic dehydrationIsotonic dehydration means that water loss is proportional to salt loss, so both the serum sodium concentration and plasma osmotic pressure are normal, but blood volume is decreased. It is also termed iso-osmotic dehydration. 4.EdemaEdema means that excessive fluid accumulates in interstitial compartment and some cavities in the body.5.HypokalemiaHypokalemia is defined as a decrease in serum K+ concentration less than 3.5 mmol/L.6.HyperkalemiaHyperkalemia is defined as an increase in serum K+ concentration more than 5.5 mmol/L.7.Hypervolemic hyponatremiaHypervolemic hyponatremia is hyponatremia with increased extracellular fluid volume resulting from excessivewater intake, meanwhile accompanied by decreased excretory function of kidney that leads to the accumulation of hypotonic fluid in exterior and interior of cells. In this situation, serum sodium concentration and plasma osmotic pressure are less than 130mmol/L and 280mmol/L, respectively, but the total amount of body sodium is normal or increased. It is also called water intoxication or hypo-osmotic overdehydration.8.PseudohyperkalemiaIn some conditions, the increase of serum K+concentration results from an artifact of laboratory measurement (due to release of potassium from blood cells during or after drawing of the blood specimen), but in fact the K+ level of plasma or serum within the body is not increased. This hyperkalemia is referred to as pseudohyperkalemia.9.Hyperpolarization blockingIn acute hypokalemia, the ICF/ECF ratio of K+ concentration increases, and the K+ efflux out of cells increases, so the voltage of the membrane potential becomes more negative than the normal resting membrane potential. At this time, the membrane becomes hyperpolarized; the difference between the resting membrane potential and the threshold potential increases with the hyperpolarization of the cell membrane; the cell membrane becomes less reactive to any stimulus that would initiate an action potential under normal circumstances. This state is referred to as hyperpolarization blocking.10.Depolarization blockingIn severe acute hyperkalemia, the resting membrane potential decreases and may fall close to the threshold potential. At this time, the cell membrane is too depolarized, which causes many voltage-gated Na+ channels to inactivate, and the action potential will not be initiated by any normal stimulus. That is, the irritability of the nerve and muscle cells is decreased. This phenomenon is termed depolarization blocking.Acid-base Balance and Imbalance1.Metabolic acidosisIt is a kind of simple acid-base disorder, which results from multiple causes and is characterized by primary reduction of [HCO3-] in plasma.2.Respiratory acidosisIt is a kind of simple acid-base disturbance,which results from the exhaust deficiency or abnormal inhale of CO2 and is characterized by primary increase of [H2CO3] in plasma or PaCO2.3.Paradoxical aciduriaIt refers to the situation that the patient with alkalemia exhibits abnormally acidic urine. Generally, the urine is basic when the patient has an alkalosis. But in the body of patient with hypokalemia, potassium ions would shift out of the cells because of low [K+] in extracellular fluid. Meanwhile, hydrogen ions outside the cells move into the cells, as a result, alkalosis in extracellular fluid ensues. At this time, because of the increase of H+and decrease of K+ in the cells, the epithelium of renal tubules secretes more H+ and less K+ into the urine to make it become abnormally more acidic.4.Paradoxical alkaluria (alkaline urine)It refers to the situation that the patient with acidemia exhibits abnormally alkaline urine. Generally, the urine is asidic when the patient has an acidosis. But in the body of patient with hyperkalemia, potassium ions would move into the cells because of high [K+] in extracellular fluid. Meanwhile, hydrogen ions in the cells move out, as a result, acidosis in extracellular fluid ensues. At this time, because of the increase of K+ and decrease of H+ in the cells, the epithelium of renal tubules secretes more K+ and less H+ into the urine to make it become abnormally more alkaline or exhibit neutral. This situation can be also found in those patients with renal tubular acidosis (RTA).5.PaCO2It refers to the partial pressure exerted by CO2 gas molecules dissolved in arterial plasma, which pressure range is normally 33~46mmHg (4.39~6.25kPa), and its average is normally 40mmHg (5.32kPa).6.Standard bicarbonate (SB)It refers to the concentration of bicarbonate in arterial plasma, which should be measured under the standard conditions. The standard conditions include a temperature of 38℃, the hemoglobin oxygen saturation of 100% and the balanced CO2 gas partial pressure of 40mmHg(5.32kPa). The normal range of this parameter is 22~27 mmol/L with an average of 24 mmol/L.7.Actual bicarbonate (AB)Under the conditions of actual hemoglobin oxygen saturation and PaCO2, the bicarbonate concentration of arterial plasma in airtight blood sample is measured. This measured parameter is termed as actual bicarbonate and reflects the actual status of an individual. Its normal value should be consistent with that of the standard bicarbonate.8.Buffer base (BB)It is the summation of all alkaline buffer substances with negative charges in blood, mainly including HCO3-, HPO42-, Pr-, Hb--, HbO2-, etc. The normal value range is 45~52mmol/L with an average of 48mmol/L9.Base excess (BE)It is a parameter measured under the standard conditions of the temperature of 38℃, the hemoglobin oxygen saturation of 100%, and PCO2 of 40mmHg. Under these conditions, the milligram molecular weight of acid or base consumed in titrating 1 litre blood or plasma sample to make its pH to 7.4. The value of base excess is positive if acid is needed, and negative if base is needed. The normal range of base excess is 0±3 mmol/L.10.Anion gap (AG)It is the deference between the concentrations of unmeasured anion (UA) and unmeasured cation (UC) in plasma (AG=UA-UC). The AG value can be obtained by calculating the difference between plasma concentration of major measured cation (Na+) and the sum of the plasma concentrations of major measured anions (Cl-and HCO3-), that is, AG = [Na+] - ([Cl-] + [HCO3-]). Its normal range is 12±2 mmol/L.11.Fixed acidsFixed acids, which are also called nonvolatile acids, are referred to as the substances which cannot be converted into gases to be removed from the body by the lungs but can be eliminated in urine by the kidneys. For example, the catabolism of some bodily substances such as certain amino acids,phospholipid and nuclear acids that contain nitrogen, sulphur and phosphorus can produce sulphuric acid, phosphoric acid and uric acid; The incomplete oxidation of carbohydrates and fats can yield some glyceric acid, pyruvic acid, lactic acid, ß-hydroxybutyric acid and acetoacetate, etc.12.Metabolic alkalosisIt is a kind of simple acid-base disorder,which is caused by multiple causes and characterized by primary increase of [HCO3-] in plasma.13.Respiratory alkalosisIt is a kind of simple acid-base disorder, which results from pulmonary hyperventilation and is characterized by primary decrease of [H2CO3] in plasma or PaCO214.Mixed acid-base disorderIt means the concurrence of two or more kinds of simple acid-base disorders in the same patient. But it is impossible that both respiratory acidosis and respiratory alkalosis occur simultaneously in the same body15.Concentrated alkalosisIt is a kind of alkalosis in which the total amount of HCO3- in the extracellular comparment does not change but its concentration rises with the decrease (or contraction) of extracellular fluid volume because of the loss of NaCl solution (e.g. administration of diuretics except the carbonic anhydrase inhibitors).16.CO2 narcosisIt refers to the situation that when PaCO2rises over 80mmHg (10.7KPa) because of the retention of CO2, the excessive high PaCO2 exerts a narcotic effect on the central nervous system.The patient with CO2 narcosis would produce those symptoms and signs including headache, fainting, dysphoria, alalia, asterixis, delirium, somnolence, twitch, even coma and respiratory inhibition, etc.17.Acid-base disturbanceAcid-base disturbance is a common basic pathological process in which, because of the actions of certain causative factors, the quantitative abnormal changes of acidic or alkaline substance within the body (overload or obvious shortage) are beyond the regulative abilities of the body, or the regulative mechanisms themselves are disrupted, or the coexistence of these two situations occurs, the normal acid-base homeostasis is damaged.ctic acidosisWhen oxygen's deficiency occurs due to various causes, glucose can be converted into lactic acid by the way of anaerobic glycolysis. If the increase of lactic acid exceeds the utilization ability of the liver, or if the lactic acid cannot be utilized sufficiently by the severely damaged liver, the concentration of lactic acid in blood will rise remarkably and a metabolic acidosis follows. At this time, the sodium bicarbonate in blood is consumed in the process of neutralizing increased hydrogen ions dissociated from lactic acid. Meanwhile, the latter's remainder, the radical of lactic acid, joins the AG. Therefore lactic acidosis is a kind of metabolic acidosis with a high AG. 19.Keto-acidosisUnder the conditions of diabetes, hunger or alcohol intoxication, etc., because of the shortage or metabolic obstruction of glucose, the catabolism of fats is accelerated so as to produce large amount of fatty acid. The latter is brought by the blood flow to the liver where it is split into ketone body. The ketone body possesses strong acidity. When the amount of ketone body exceeds the oxidative ability of peripheral tissue as well as the removal ability of the kidneys, it would be accumulated in the blood and this situation is then called keto-acidosis, which belongs to the kind of metabolic acidosis with a high AG.20.Renal tubular acidosis (RTA)It is a kind of disorder that mainly results from a defect in renal tubular excretion of hydrogen ion or in reabsorption of bicarbonate, or both. The main causes of this disorder include chronic renal failure, insufficient aldosterone secretion (Addison's disease), and some hereditary or acquired disorders leading to decreased renal tubular function, such as Fanconi's syndrome etc. Nevertheless the glomerular function maintains normal. Under this situation, serious acidemia can occur while the urine is paradoxically alkaline or neutral.Hypoxia1.HypoxiaHypoxia can be defined as a deficiency in either oxygen delivery or its utilization at the tissue level or the deficiency of both, which can lead to changes in function, metabolism and even structure of the body.2.CyanosisCyanosis refers to the violaceous color of skin and mucous membranes which occurs as the deoxyhemoglobin concentration of the blood in capillaries becomes greater than 5g/dl.3.Hemic hypoxiaHemic hypoxia refers to hypoxia resulting from a low carrying capacity of oxygen in the blood caused by an altered affinity of Hb for oxygen or a decrease in the amount of Hb in the blood.4.Enterogenous cyanosisWhen pickled vegetables containing nitrate are consumed in large amounts, the reabsorbed nitrate reacts with HbFe2+to form HbFe3+OH. The color of skin becomes coffee color. This phenomenon is called enterogenous cyanosis.5.Partial pressure of oxygen (PO2)PO2 is the tension produced by oxygen molecules physically dissolved in plasma.6.Oxygen binding capacity of hemoglobin (CO2max)CO2max is the maximal amount of O2 that can be potentially combined to hemoglobin in 100ml blood.7.Oxygen content in blood (CO2)CO2is the actual oxygen content in 100ml blood, including oxygen combined to Hb and oxygen physically dissolved in plasma (only 0.3ml/dl).8.Oxygen saturation of hemoglobin (SO2)SO2 is the percentage of haemoglobin present as oxyhaemoglobin, normally 97~99% in arterial blood and about 75% in venous blood.9.Ischemic hypoxiaThe deficiency of blood perfusion to tissues caused by decreased arterial pressure or obstruction of arteries is called ischemic hypoxia.Fever1.FeverFever is a complicated pathological process characterized by a regulated elevation of core body temperature, in which the hypothalamic set point is temporarily reset at an elevated temperature in response to pyretic substances.2.Pyrogenic activatorsFever can be caused by a number of microorganisms and non-microbial pyretic substances, which are collectively called pyrogenic activators.3.Endogenous pyrogensEndogenous pyrogens are described as cytokines inducing fever, which are produced and released by EP cells, such as interleukin-1, tumor necrosis factor, etc.4.HyperthermiaHyperthermia is described as the elevation of body temperature that occurs without changes of the set point in the hypothalamic thermoregulatory center. It occurs when the thermoregulatory mechanisms are overwhelmed.5.Exogenous pyrogensMicroorganisms and their products are also called exogenous pyrogens.Stress1.StressIt is defined as a systemic nonspecific response of the body to environmental demands or pressures made upon it.2.General adaptation syndromeIt refers to a series of physiological, psychological and behavioral adaptive responses of the body after its homeostasis is threatened and disturbed. When the stressor continues its effect on the body, general adaptation syndrome manifest a dynamic, continuous process, and can finally lead to collapse of adaptive mechanism, occurrence of diseases and even death. General adaptation syndrome is a collective term for various damages and injuries of the body caused by stress response.3.Heat shock proteinsHeat shock proteins are a family of stress proteins which synthesis is elicited or up-regulated in response to a variety of stimuli such as “heat stress”. They are considered intracellular, and non-secreted proteins which functions include helping the proper folding of newly synthesized proteins and guiding their movement, helpingthe repair, removal, and proteolysis of damaged proteins.4.StressorThe stimulus that provokes a stress response is referred to as stressor.5.Acute phase proteinIn response to stressors, such as infection, inflammation, or tissue injuries, the body is elicited to evoke rapid-mobilized defensive and non-specific responses, such as rise of body temperature, raised level of blood glucose, increase of white blood cell amounts, nuclear left shift, and increase of some plasma protein concentrations. The responses listed above are called “acute phase responses”. And the plasma proteins which level in plasma increase quickly is called 'acute phase proteins' and are secreted proteins.6.Molecular chaperoneIt is also termed as “heat shock protein”. It can participate in the proper folding, movements and maintenance of newly synthesized proteins. It also can recognize and bind to the exposed hydrophobic domain of denatured proteins to prevent them from aggregating. Then it will help the protease system produce proteolystic effects on those proteins or refold them into nature conformation.Shock1.ShockShock is a pathological process caused by various drastic etiological factors, which is characterized by microcirculation failure resulting from decreased effective circulatory blood volume and inadequate tissue perfusion with the results of cellular metabolism impediment and dysfunction of multiple vital organ.2.Auto blood transfusionAt the early stage of shock, vessel constriction because of release of a large amount of vasoconstrictors may mobilize the stored blood to participate in the circulation, which is considered as compensation of venous return.3.Auto fluid transfusionAt the early stage of shock, significant decrease of hydrostatic pressure in capillary may drive fluid to shift from interstitial space to the vascular compartment, and as a result, the plasma volume can be partly restored as a compensatory responseCoagulation-Anticoagulation Balance and Imbalance1.3P test3P test is a test for detecting fragment X of FDP. Normal serum contains no detectable level of FDP. In patient with DIC, the activated fibrinolysis can result in an increase in fragment X of FDP which usually combines with fibrinmonomer to form soluble fibrinmonomer complex. Fragment X may dissociate from the soluble complex and then fibrinmonomers are polymerized to form gelatinous fibrin precipitate in the presence of protamine. The positive result of 3P test indicates the activation of fibrinolysis and the presence of DIC.2.Disseminated intravascular coagulation (DIC)DIC is a pathological process caused by disturbance of the kinetic balance between coagulation and anticoagulation systems (including fibrinolytic system). Etiologic factors activate extensive intravascular coagulation and secondary fibrinolysis. The clinical features of DIC are bleeding, shock, organ dysfunction and microangiopathic hemolytic anemia.3.Fibrin degradation products (FDP)Fibrinolysis is initiated by fibrin clot and plasminogen activator in DIC. Plasmin can degrade fibrin to form a series of protein fragments, called fibrin degradation products (FDP). FDP may act as antithrombin to inhibit coagulation process.Heart failure1.Heart failureHeart failure is a pathological process in which the systolic or/ and diastolic function of the heart is impaired, and as a result, cardiac output decreases and is unable to meet the metabolic demands of the body.2.High-output failureHigh-output failure indicates that the cardiac output may be supra- normal but inadequate owing to excessive metabolic needs. The causes of high-output heart failure include severe anemia, fever, hyperthyroidism and pregnancy, etc.3.Myogenic dilationThe heart is overfilled to such an extent that the contractility produced by the slide of actin and myosin filaments decreases, with the result, the further increase of ventricular filling may produce a decrease in cardiac output. This kind of cardiac dilation is called myogenic dilation.4.Concentric hypertrophyIt is a type of myocardial hypertrophy. It, as a myocardial response to pressure overload, is associated with increased numbers of sarcomeres arranged in parallel (parallel hyperplasia of myocardial fibers) which lead to an increase in cardiac wall thickness without the increase of internal chamber size.5.Eccentric hypertrophyIt is a type of myocardial hypertrophy and it, as a myocardial response to volume overload, results from increased numbers of sarcomeres arranged in series (series lengthening of myocardial fibers) which produce an decrease in cardiac wall thickness with increase of internal chamber size.6.OrthopneaOrthopnea refers to shortness of breath that occurs when the patient with heart failure and pulmonary circular congestion is lying down in a horizontal position. Because of that, the patient has to sit up in a forward-leaning posture or by supporting the back of his/her body with several pillows so as to lessen dyspnea. The horizontal position redistributes body fluid, increases blood return from the extremities, leads to abdominal contents to exert pressure on the diaphragm, or reduces the efficiency of the respiratory muscles.7.Paroxysmal nocturnal dyspneaParoxysmal nocturnal dyspnea is a sudden attack of dyspnea that occurs during sleep in a recumbent posture. The patients with left heart failure wake up at night gasping for air and have to sit up or stand to relieve the dyspnea. It is precipitated by the development of interstitial pulmonary edema because of the redistribution of body fluid.8.Myocardial remodelingMyocardial remodeling is a process based on the alteration of gene expression involving myocardial cells, non-myocardial cells and extracellular matrix (ECM). It includes myocardial hypertrophy and phenotype alteration, non-myocardial cellular proliferation and ECM rebuilding.Respiratory Failure1.Dead space like ventilationIt indicates that the blood flow in the ventilated alveoli is reduced because of diseases. So the air in these alveoli cannot be exploited sufficiently. This situation is just like dead space ventilation.2.Functional shuntBecause of obstructive or restrictive ventilation dysfunction, the involved alveoli have hypoventilation but their blood flow does not reduce, thus the ratio of V A/Q is lowered, leading to the venous blood passing through the alveolar capillaries to flow into pulmonary vein without enough oxygenation. This condition is called venousadmixture, just like artery-vein shunt.3.Pulmonary encephalopathyIt means the central nervous system dysfunction resulting from chronic respiratory failure. The reason why it occurs is that hypoxia, hypercapnia and acidosis produce the damage effects on the cerebral vessels and cerebral cells, resulting in cerebral vasodilation, the increases in cerebral blood flow and cerebral vascular permeability, the edema and electric activity dysfunction of brain cells and intracellular lysosomal enzyme release.4.Acute respiratory distress syndrome (ARDS)It is a pathological process caused by severe shock, infection and intoxication, et al. Its basic pathological change is the acute injuries of alveolar- capillary membrane. ARDS induces acute respiratory failure, characterized by progressive dyspnea and refractory hypoxemia.5.Respiratory failureRespiratory failure is a syndrome, in which the severe external respiratory dysfunction leads to a PaO2 below 60 mmHg (8.0kPa) with or without a PaCO2 above 50 mmHg (6.67kPa) in a resting subject breathing air at sea level.6.Restrictive hypoventilationIt means hypoventilation caused by the restriction of alveolar dilation or inflation during inspiration.7.Obstructive hypoventilationIt means hypoventilation that caused by the stenosis or obstruction of airway and the increased airway resistance.Hepatic Failure1.Hepatic insufficiencyHepatic insufficiency is referred to a syndrome, in which severe liver damage results in severe dysfunctions, including jaundice, bleeding, infection, renal dysfunction or encephalopathy.2.Hepatic failureHepatic failure is a terminal stage of hepatic insufficiency. Hepatic encephalopathy and hepatorenal syndrome are the primary clinical manifestations.3.Hepatic encephalopathyHepatic encephalopathy is a complex, potentially reversible disturbance in central nervous system that occurs as a consequence of severe liver diseases. It is characterized by neuropsychical manifestations ranging from a slightly altered mental status to coma.4.Gamma-aminobutyric acid (GABA) hypothesisGamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central nervous system. Increased GABA is observed in patients with cirrhosis, perhaps because of decreased hepatic metabolism of GABA When GABA crosses the blood-brain barrier of patients with cirrhosis, it interacts with supersensitive postsynaptic GABA receptors. Activation of the GABA receptor increases neuronal membrane permeability to Cl-by opening the Cl- ionophore. When the Cl- resting potential of the neurons is more negative than the neuronal resting membrane potential, Cl- will enter the neurons causing membrane hyperpolarization, thus leading to the dysfunction of CNS.5.Ammonia intoxication hypothesisAmmonia intoxication hypothesis holds that the patient with hepatic cirrhosis has hyperammonemia and the occurrence of hepatic encephalopathy is due to entering of ammonia into the brain. All of the neuropsychiatric symptoms are due to the poisonous action of ammonia to central nervous system.6.False neurotransmitter hypothesisIn the patient with hepatic failure, false neurotransmitters are accumulated in the synapse of the reticular structure in the brain stem. The false neurotransmitters can compete with true neurotransmitters because their chemical structure is similar to the true neurotransmitters. When false neurotransmitters replaces true neurotransmitter inthe reticular structure, the disorders of CNS occur.Renal Failure1.Renal osteodystrophyRenal osteodystrophy is a serious complication of CRF (especially, of uremia), which includes renal rickets (for children), adult osteomalacia, osteitis fibrosa, osteoporosis, osteosclerosis, and etc.2.Trade-off hypothesisTrade-off hypothesis indicates that as the nephrons are progressively destroyed, increased blood concentration of some solutes stimulate over-secretion of some related regulatory factors (such as hormones) in order to increase the excretion function. At the same time, however, high blood levels of the regulatory factors will result in some other metabolic disorders.3.UremiaIt comes from the Greek 'urine in the blood'. Uremia is a clinical and biochemical syndrome that occurs either abruptly or gradually as renal function declines acutely or chronically. Uremia is the end-stage of renal failure, with which the patients have to receive treatment in the form of dialysis or renal transplantation.4.Acute renal failure (ARF)Acute renal failure is a pathological progress, which is characterized by a deterioration of renal function over a period of hours to days, resulting in failure of kidney to excrete nitrogenous waste products and to maintain fluid, electrolyte homeostasis and acid-base balance. The patients often present azotemia, water intoxication, hyperkalemia and metabolic acidosis.5.Chronic renal failure (CRF)Chronic renal failure is a syndrome of impaired homeostasis owing to structural damage (reduced functional nephrons) of the kidneys. The disturbances are characterized by metabolic acidosis, hypocalcemia, hyperphosphatemia, alteration in vitamin D metabolism and the presence of certain toxic materials in body fluid.Ischemia- reperfusion injury1.Ischemia- reperfusion injuryThe restoration of blood flow after transient ischemia may be associated with further reversible or irreversible cell damage, which is called ischemia-reperfusion injury or reperfusion injury.2.Calcium overloadCalcium overload refers to that intracellular content of calcium is increased abnormally during ischemia and reperfusion, which results in the disorder of cellular structure and function.3.No-reflow phenomenonNo-reflow phenomenon refers to a paradoxical phenomenon that the relief of blood vessel occlusion (or other causes responsible for ischemia) cannot make the ischemic area obtain sufficient blood perfusion. The significant impairment of flow may occur at microvascular level. The main determinant of no-reflow is the activation of neutrophils in microvesseles.4.Respiratory burstNeutrophils (NADPH oxidase etc) activated by ischemia may obviously increase the production of oxygen free radicals (e.g., O2-·, H2O2) during reperfusion regaining O2 supplement, the phenomenon is called respiratory burst.5.Oxygen paradoxOxygen paradox refers to that the restoration of the oxygen partial pressure in perfusion solution after transient hypoxia may be associated with increase in membrane permeability and cell death.。

肺移植术后原发性移植物功能障碍的危险因素研究进展

肺移植术后原发性移植物功能障碍的危险因素研究进展

第12卷 第3期2021年5月Vol. 12 No.3May 2021器官移植Organ Transplantation肺移植是治疗终末期肺疾病的唯一有效方式,但国际心肺移植学会(International Society for Heart and Lung Transplantation ,ISHLT )报告显示,肺移植受者的早期预后远不如其他实体器官移植受者,术后中位生存期仅6.7年,其中原发性移植物功能障碍(primary graft dysfunction ,PGD )是影响其预后的【摘要】 肺移植是治疗终末期肺疾病的唯一有效方式,但肺移植受者的早期预后远不如其他实体器官移植受者,其中原发性移植物功能障碍(PGD )是影响其预后的主要原因之一。

PGD 是肺移植术后早期发生的一种急性肺损伤,是导致肺移植受者术后早期死亡的主要原因。

肺移植受者术后PGD 发生的危险因素包括供者、受者、手术等多方面。

本文对肺移植术后发生PGD 的危险因素进行综述,旨在为临床提供参考。

【关键词】 肺移植;原发性移植物功能障碍;扩大标准供者;活性氧簇;体外膜肺氧合;体外肺灌注;体外 循环;输血相关性肺损伤【中图分类号】R617,R563 【文献标志码】A 【文章编号】1674-7445(2021)03-0016-06·综述·肺移植术后原发性移植物功能障碍的危险因素研究进展胡春兰 于慧智 王净 李小杉 胡春晓【Abstract 】 Lung transplantation is the only effective approach to treat end-stage lung diseases. Nevertheless, early prognosis of lung transplant recipients is significantly worse than that of other solid organ transplant recipients. Primary graft dysfunction (PGD) is one of the main causes affecting clinical prognosis of the recipients. PGD is an early acute lung injury after lung transplantation, which is the main cause of early death of lung transplant recipients. Risk factors of PGD after lung transplantation consist of donor, recipient and operation, etc . In this article, the risk factors of PGD after lung transplantation were reviewed, aiming to provide reference for clinical practice.【Key words 】 Lung transplantation; Primary graft dysfunction; Expanded criteria donor; Reactive oxygen species; Extracorporeal membrane oxygenation; Ex vivo lung perfusion; Cardiopulmonary bypass; Transfusion-related lung injuryResearch progress on risk factors of primary graft dysfunction after lung transplantation Hu Chunlan *, Yu Huizhi, Wang Jing, Li Xiaoshan, Hu Chunxiao. *Department of Anesthesiology, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi 214023, ChinaCorrespondingauthor:HuChunxiao,Email:***********************DOI: 10.3969/j.issn.1674-7445.2021.03.016基金项目:国家自然科学基金(8207011015);无锡市卫生健康委青年项目(Q202003)作者单位:214023 江苏无锡,南京医科大学附属无锡人民医院麻醉科(胡春兰、王净、于慧智、李小杉、胡春晓),肺移植中心 (胡春晓)作者简介:胡春兰,女,1995 年生,硕士研究生,住院医师,研究方向为肺缺血-再灌注损伤和移植物功能研究,Email: huchunlan *************通信作者:胡春晓,男,1971 年生,主任医师,研究方向为肺缺血-再灌注损伤、重要器官功能保护和 ECMO 辅助下肺移植围手术期的应用管理及脑损伤的机制,Email:***********************·358·第12卷器官移植主要原因之一。

英文:硫辛酸改善PC12细胞中GSH的水平:帕金森治疗的新启示

英文:硫辛酸改善PC12细胞中GSH的水平:帕金森治疗的新启示

Pre-treatment with R -Lipoic Acid Alleviates the Effects of GSH Depletion in PC12Cells:Implications for Parkinson’sDisease TherapyS.Bharath 1,*,B.C.Cochran 1,M.Hsu 1,J.Liu 2,3,B.N.Ames 2,3,J.K.Andersen 11Buck Institute for Age Research,8001Redwood Blvd.,Novato,CA 94945,USA2Division of Biochemistry and Molecular Biology,University of California,Berkeley,CA 94720,USA 3Children’s Hospital Oakland Research Institute,Oakland,CA 94609,USAReceived 22August 2001;accepted 12April 2002AbstractOxidative stress is believed to play a key role in the degeneration of dopaminergic neurons in the substantia nigra (SN)of Parkinson’s disease (PD)patients.An important biochemical feature of PD is a significant early depletion in levels of the thiol antioxidant compound glutathione (GSH)which may lead to the generation of reactive oxygen species (ROS),mitochondrial dysfunction,and ultimately to subsequent neuronal cell death.In earlier work from our laboratory,we demonstrated that depletion of GSH in dopaminergic PC12cells affects mitochondrial integrity and specifically impairs the activity of mitochondrial complex I.Here we report that pre-treatment of PC12cells with R-lipoic acid acts to prevent depletion of GSH content and preserves the mitochondrial complex I activity which normally is impaired as a consequence of GSH loss.#2002Elsevier Science Inc.All rights reserved.Keywords:Parkinson’s disease;Glutathione (GSH);R -lipoic acid;Mitochondrial complex IINTRODUCTIONParkinson’s disease (PD)is a progressive,neurode-generative disorder which involves the loss of dopa-minergic neurons of the substantia nigra (SN)pars compacta (Beal,1992)The disease condition occurs mostly in late midlife with clinical features including motor impairment,gradual loss of cognition,and depression.Oxidative stress appears to play an impor-tant role in neuronal degeneration associated with PD (Beal,1992;Burke,1998;Adams et al.,2001;Sayre et al.,2001).Dopaminergic neurons are particularly prone to oxidative stress due to oxidation of dopamine leading to the generation of reactive oxygen species(ROS).ROS act to oxidize various biological macro-molecules thereby disturbing homeostasis within the cell ultimately leading to cell death (Beal,1992;Burke,1998;Adams et al.,2001;Sayre et al.,2001).It has been observed that the SN of early PD patients has significantly decreased levels of glutathione (GSH)(Perry and Yong,1988).GSH is a tripeptide localized both within the cytoplasm and mitochondria of neurons and other cell types.It acts as the major non-proteinac-eous antioxidant and redox modulator within the brain.The depletion of GSH in the SN is the earliest known indicator of oxidative stress in presymptomatic PD,preceding both decreases in mitochondrial complex I activity and dopamine levels (Jenner,1993).GSH is synthesized by a two-step reaction involving the enzymes g -glutamyl cysteine ligase (g -GCL)and glutathione synthetase.g -GCL is the rate-limiting enzyme in this process and brain GSH appearstoNeuroToxicology 23(2002)479–486*Corresponding author.Tel.:þ1-415-209-2000;fax:þ1-415-209-2231.E-mail address :bsrinivas@ (S.Bharath).0161-813X/02/$–see front matter #2002Elsevier Science Inc.All rights reserved.PII:S 0161-813X (02)00035-9primarily arise through synthesis from its constituent amino acids via this enzyme(Meister,1988).g-GCL is a dimer composed of a heavy catalytic subunit and a light regulatory subunit(Huang et al.,1993).GSH is synthesized in the cytosol and transported into the mitochondria via an energy-dependent transporter (Meister,1988).In earlier studies from our laboratory, we reported on the effects of partial depletion of GSH levels via g-GCL inhibition on mitochondrial physio-logy in PC12cells(Jha et al.,2000).When GSH levels in PC12were down regulated by simultaneous dox-ycycline(Dox)-induced expression of antisense g-GCL light and heavy subunit mRNAs and protein levels, it resulted in decreased mitochondrial GSH levels, increased oxidative stress,and decreased mitochon-drial function.Decreased mitochondrial activity in these cells appeared to be due to a selective inhibition of complex I activity as a result of thiol oxidation of the enzyme complex.These results suggested that the early observed GSH losses in the SN of PD patients could be linked to decreases in complex I activity(via increased ROS)and subsequent mitochondrial dysfunction which ultimately leads to dopaminergic cell death associated with the disease(Jha et al.,2000;Beal,1992).R-lipoic acid plays a fundamental role in mitochon-drial metabolism as a coenzyme for pyruvate dehy-drogenase and alpha-ketoglutarate dehydrogenase and as a substrate for the NADPH-dependent enzyme glutathione reductase.In recent years,R-lipoic acid has received considerable attention as an antioxidant (Fuchs et al.,1997;Packer et al.,1995;Sen et al., 1999).It has been demonstrated to have neuroprotec-tive effects on neuronal cells(Wolz and Krieglstein, 1996,1997;Tirosh et al.,1999;Sen et al.,1998). Studies using both in vitro and in vivo models have suggested that pretreatment with R-lipoic acid increases cellular levels of GSH,probably by prevent-ing its depletion thereby protecting mitochondrial integrity(Suzuki et al.,1991;Scott et al.,1994;Han et al.,1997;Xu and Wells,1996;Lykkesfeldt et al., 1998;Kagen et al.,1992).To address the question of the possible mechanism of R-lipoic acid-mediated protection,we have analyzed the effect of pretreatment with R-lipoic acid on GSH-depleted PC12cells.We have used buthionine sulfox-imine(BSO),an irreversible inhibitor of the enzyme g-GCL,to decrease GSH levels within PC12.BSO is a widely used pharmacological agent for decreasing GSH content in peripheral tissues as well as in cell culture models(Minchinton et al.,1984;Lee et al., 1988;Thanislass et al.,1995;Andersen et al.,1996). We demonstrate that pre-treatment of GSH-depleted cells with R-lipoic acid prevents depletion of the GSH pool within the cytoplasm and mitochondria.We also show that this pretreatment leads to preservation of mitochondrial complex I activity lost due to GSH depletion.MATERIALS AND METHODSPC12cells were obtained from American Type Culture Collection(ATCC),Rockville,MD.All tissue culture materials were procured from Life Technolo-gies or Cellgro.Chemicals were obtained from Sigma Chemical Company.The GSH assay kit was obtained from OXIS Research Inc.R-lipoic acid was a gift from ASTA Medica(Frankfurt/Main,Germany).Cell CulturePC12cells were cultured in DMEM medium con-taining10%horse serum,5%fetal bovine serum(FBS) and antibiotics(2units penicillin/ml and0.02mg streptomycin/ml)at378C and5%CO2.Cells were subcultured once a week by gentle cell scraping.Stock solutions of buthionine-S,R-sulfoximine(BSO)and R-lipoic acid were prepared in Hanks balanced salt solution(HBSS).Preparation of MitochondriaMitochondria were prepared by the method of Trounce et al.(1996).Briefly,PC12cells were har-vested,washed in Buffer H(5mM HEPES,210mM mannitol,70mM sucrose,1mM EGTA and0.5% BSA)then resuspended in the same buffer.The cell suspension was then homogenized and centrifuged at 800Âg for5min at48C.The supernatant which was enriched in mitochondria was then centrifuged at 10,000Âg for20min at48C.The resultant mitochon-drial pellet was resuspended in buffer H and stored as aliquots atÀ208C.Estimation of Total Glutathione(GSHþGSSG) in Whole Cells and MitochondriaTotal cellular and mitochondrial glutathione estima-tion was carried out using a kit from OXIS Research Inc.following the instructions provided by the manu-facturer.Cells were plated at1Â106cells/ml in either 6-well dishes or90mm diameter plates.All estima-tions were conducted in triplicate.Cells were incubated with BSO and/or R-lipoic acid for the indicated time intervals at378C.Cells were then harvested,disrupted480S.Bharath et al./NeuroToxicology23(2002)479–486by sonication and cellular proteins precipitated by tricholoroacetic acid.The soluble fraction,which is enriched for total glutathione,was estimated using the OXIS kit.Briefly,samples werefirst buffered and then the reducing agent,tris(2-carboxyethyl)phosphine (TCEP)was added to reduce any oxidized glutathione (GSSG).The chromogen4-chloro-1-methyl-7-trifluor-omethylquinolinium methylsulfate was then added which forms thioethers with all thiols present in the sample.Upon addition of base to raise the pH to greater than13,a b-elimination specific to the GSH-thioether results in a chromophoric thione.The absorbance of this thione measured at420nm is directly proportional to total glutathione concentration.All values obtained were normalized per protein and tabulated. Mitochondrial Complex I Enzyme Assay Complex I enzyme assays were carried out as described by Trounce et al.(1996).Briefly,the assay was initiated by addition of aliquots of sonicated cell samples to50mM potassium phosphate pH7.4, 500m M EDTA,1%BSA,200m M NADH and200m M decylubiquinoneþ2m M rotenone in the presence of KCN with0.002%dichloroindophenol(DCIP)as a secondary electron acceptor.The decrease in the absorbance at600nm was recorded as a measure of enzyme reaction rate at308C for10min and specific activity was calculated.The results were plotted as relative rotenone-sensitive specific activity.c-Glutamyl Cysteine Ligase Enzyme Assayg-GCL assays were carried out as described by Seelig and Meister(1985).Briefly,cells obtained after various treatments were washed in1ÂPBS and resuspended in0.1M Tris–HCl,pH8.0.The cell suspension was sonicated and used as a source for g-GCL enzyme activity.The enzyme activity was determined at378C by adding cell lysates to a reaction mixture containing0.1M Tris–HCl buffer,pH8.0, 150mM KCl,5mM sodium ATP,2mM phosphoenol-pyruvate,10mM L-glutamate,10mM a-amino buty-rate,20mM MgCl2,2mM EDTA,0.2mM NADH, 17U pyruvate kinase and17U lactate dehydrogenase. The absorbance at340nm was monitored as a measure of enzyme activity.Assays run in the absence of a-aminobutyrate served as blank.All the g-GCL activ-ity values were normalized per protein.RESULTSPC12cells represent a good model system for the study of oxidative stress in dopamine-containing cells as they exhibit several physiological properties of dopaminergic neurons(Greene and Tischler,1976). PC12cells were treated with100m M of BSO for different time points and total glutathione content measured.Following BSO treatment,there was a gradual decrease in the levels of total cellular GSH content with time(Fig.1);the maximum decrease was observed at24h(data not shown).For subsequent experiments,addition of100m M of BSO for a time period of6h was employed to maintain approximately 50%depletion in total cellular GSH content,similar to the decreases observed in the PD SN.The unbound form of R-lipoic acid has two–SH groups and has been found to be an effective thiol anti-oxidant(Suzuki et al.,1991;Scott et al.,1994;Han et al.,1997;Xu and Wells,1996;Lykkesfeldt et al., 1998;Kagen et al.,1992).Therefore,R-lipoicacid Fig.1.The effect of100mM BSO on total cellular glutathione levels in PC12cells at various time points.Significance of difference fromthe control was determined by ANOV A single factor analysis.Data is expressed as meanÆS:E:M:(n¼3).ÃP<0:005vs.untreated cells;ÃÃP<0:001vs.untreated cells.S.Bharath et al./NeuroToxicology23(2002)479–486481pretreatmentwas testedtoseeifthiscould helpovercome the dramatic decreases in BSO-induced glutathione levels.PC12cells were incubated with 100m M of freshly prepared R -lipoic acid for 24h and then sub-jected to BSO treatment for 6h as previously described.Pretreatment with R -lipoic acid prevents depletion of glutathione levels within BSO-treated PC12cells (Fig.2a ).Mitochondrial glutathione content estimated from BSO-treated cells pre-treated with R -lipoic acid versus untreated cells demonstrate that mitochondrial levels of glutathione were decreased as signi ficantly as cellular glutathione levels by BSO treatment and that they too are completely preserved upon pre-treatment with R -lipoic acid (Fig.2b ).These results emphasize the role of R -lipoic acid as a potential anti-oxidant with the ability to help cells maintain their total GSH pool.It has been well documented in PD that mitochon-drial dysfunction is a hallmark of disease pathogenesis (Beal,1992).This abnormality is manifested by a selective decrease in the enzymatic activity of mitochondrial complex I (Beal,1992;Jenner,1993;Hillered and Chan,1988;Haas et al.,1995;Jha et al.,2000).Since pretreatment with R -lipoic acid signi fi-cantly prevented BSO-mediated depletion of cellular and mitochondrial total glutathione levels,it was logi-cal to analyze whether this type of pretreatment could lead to preservation of mitochondrial complex I activ-ity following BSO treatment.Hence,mitochondrial complex I enzyme assays were carried out on cells which had been pretreated with R -lipoic acid versus un-pretreated cells prior to BSO application.Fig.3shows data demonstrating that pre-incubation ofPC12Fig.2.The effect of pre-treatment with 100mM R -lipoic acid on the total glutathione (GSH þGSSG)levels in BSO treated and untreated (a)whole cell extracts and (b)mitochondria.Significance of difference from control was determined by ANOV A single factor analysis.Data is expressed as mean þS :E :M :(n ¼3).(a)ÃP <0:0001vs.untreated cells;ÃÃP <0:0001vs.untreated cells;ÃÃÃP <0:001vs.BSO alone treated cells.(b)ÃP <0:001vs.untreated cells;ÃÃP <0:0001vs.untreated cells;ÃÃÃP <0:005vs.BSO alone treatedcells.Fig.3.The effect of pre-treatment with 100m M R -lipoic acid on mitochondrial complex I activity in BSO-treated and untreated PC12cells.Relative rotenone-sensitive specific activities are plotted.Significance of difference from control was determined by ANOV A single factor analysis.Data is expressed as mean ÆS :E :M :(n ¼6).ÃP <0:005vs.control.482S.Bharath et al./NeuroToxicology 23(2002)479–486cells with R -lipoic acid preserves impaired complex I activity caused by BSO insult.The effect of R -lipoic acid demonstrated here might be due to either an increase in the activity of g -GCL,the rate-limiting enzyme in the glutathione production,or due to the direct anti-oxidant activity of R -lipoic acid which may prevent glutathione depletion.To distinguish between these two,we carried out enzyme assays for g -GCL from extracts obtained after various treatments.The result of these experiments (Fig.4)demonstrate that upon BSO treatment alone there is a decrease ($50%)in the g -GCL activity whereas cells treated with either R -lipoic acid alone or R -lipoic acid þBSO do not show any difference in the activity compared to control cells.DISCUSSIONOne of the earliest detectable events during the course of PD is a signi ficant decrease in cellular levels of GSH in the SN (Pearce et al.,1997;Jenner,1993).This may contribute to oxidative stress and ensuing neuronal cell death of dopaminergic neurons in this brain region.Based on our earlier published findings,we proposed that early GSH depletion in the SN may be directly responsible for selective inhibition of mito-chondrial complex I activity and the concomitant loss of mitochondrial function which leads to neuronal cell death in this disorder (Jha et al.,2000).Selective reductions in GSH levels which precede losses in mitochondrial complex I activity have been reported to occur not only in PD but also in associated toxin models of the disease such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)administration (Perry and Yong,1988;Hallman et al.,1985;Sriram et al.,1998).Whether the inhibition of complex I activity and subsequent decreases in ATP levels fol-lowing MPTP administration can be totally accounted for by decreases in GSH levels is unclear as complex I also appears to be directly inhibited by interaction with 1-methyl-4-phenyl pyridium (MPP þ)formed during monoamine oxidase-B-mediated oxidation of MPTP (Jha et al.,1999).However,decreasing GSH levels by treatment with the pharmacological agent BSO has been shown to potentiate the neurodegenerative effects of MPTP in the SN and to alone cause sublethal damage to the nigrostriatal system (Wullner et al.,1996;Andersen et al.,1996).GSH is an anti-oxidant molecule well known to protect proteins during oxidative stress.It acts by conjugating oxidized thiol groups of target proteins forming mixed disul fides which are then processed by GSH reductase,thioredoxin or protein disulphide isomerase to reduced protein thiol residues and GSH (Ravindranath and Reed,1990;Jung and Thomas,1996).Thus,GSH serves as a major non-protein cellular defense against oxidative stress by maintaining the reduced state of cellular thiol proteins.Since GSH depletion in the SN is well documented in PD,it is of paramount importance to search for and test com-pounds which could prevent depletion of cellular levels of GSH in PD patients.To screen for such compounds,we have utilized the PC12cell culture model system in which activity of g -GCL has been partially impaired by BSO treatment.Although g -GCL activity levels do not appear to be speci fically impaired in sporadic cases of PD,the overall effect of BSO treatment in the dopaminergic PC12cells mimics that which is seen in the Parkinsonian brain,i.e.a decrease in GSHlevelsFig.4.The effect of pre-treatment with 100m M R -lipoic acid on g -glutamyl cysteine ligase activity in BSO-treated and untreated PC12cells.Relative %specific activity is plotted.Significance of difference from control was determined by ANOV A single factor analysis.Data is expressed as mean ÆS :E :M :(n ¼6).ÃP <0:0001vs.control.S.Bharath et al./NeuroToxicology 23(2002)479–486483leading to increased oxidative stress(Wullner et al., 1996;Andersen et al.,1996).Furthermore,though acute depletion of GSH appeared to have no effect on overall cell viability or growth even after48h(Jha et al.,2000),prolonged mitochondrial dysfunction would likely eventually result in decreased cell viability like that observed in dopaminergic SN neurons in PD. As shown in Figs.1and2,increased exposure to BSO results in a notable decrease in the GSH content both in whole cell preparations and in the mitochondria. Significant changes occur in the mitochondrial phy-siology during oxidative stress and in diseases like PD (Beal,1992).In this current study,we found that BSO treatment eliciting an increase in oxidative stress via a 50%decrease in total cellular GSH content resulted a 40%decrease in the specific activity of mitochondrial complex I(Fig.3).This correlates well with our earlier findings in which we observed a similar decrease in mitochondrial complex I activity following50%GSH depletion,with no apparent effects on the activities of the other mitochondrial complexes(Jha et al.,2000). Mitochondrial complex I is considered to be the mitochondrial complex the most severely affected by oxidative stress(Lenaz et al.,1997).In synaptic mitochondria,complex I exerts a major control over oxidative phosphorylation such that at only25%inhi-bition,energy metabolism is disturbed resulting in decreased ATP synthesis(Davey et al.,1998).R-lipoic acid,a thiol containing compound,is a widely used antioxidant(Fuchs et al.,1997;Packer et al.,1995;Sen et al.,1999).R-lipoic acid functions as a redox regulator of proteins such as myoglobin, prolactin,thioredoxin,and NF-kappa B transcription factor(Bushtamante et al.,1998;Packer et al.,1995, 1997).It has been utilized to treat or prevent peripheral neuropathy and cardiac autonomic neuropathy(Ziegler and Gries,1997),insulin resistance in type II diabetes (Jacob et al.,1996),retinopathy and cataracts(Maitra et al.,1996),glaucoma(Head,2001),HIV/AIDS (Packer et al.,1995),cancer(Ames,1999),liver disease (Bushtamante et al.,1998),Wilson’s disease(Yamamoto et al.,2001),cardiovascular disease(Matalon et al., 1984)and lactic acidosis caused by inborn errors of metabolism(Yoshida et al.,1990).It has also been used for treatment of Alzheimer type dementia(Hager et al., 2001).R-lipoic acid administration has been reported to result in increased ambulatory activity and improved memory in aged animals and to partially restore age-associated mitochondrial decay in both the liver and heart(Hagen et al.,1999,2000;Suh et al.,2001). It therefore seems likely that thiol antioxidants such as R-lipoic acid which can enhance mitochondrial function,scavenge free radicals,and increase the levels of the antioxidants GSH and ascorbate might be useful neuroprotective agents via their reducing actions onvital protein thiol residues(Han et al.,1997;Xu and Wells, 1996).Our results together with previous studies suggest that R-lipoic acid may be an effective neuroprotective agent in age-associated neurodegeneration.Utilizing the PC12cell model system,we propose that R-lipoic acid administration could be an effective way of circumventing or delaying mitochondrial dys-function associated with PD.Treatment with R-lipoic acid alone seems to significantly increase GSH levels only in whole cell preparations but not in mitochon-drial extracts(see Fig.2a and b).However,pretreat-ment of cells with R-lipoic acid appears to prevent BSO-mediated GSH depletion in both whole cells and mitochondria.These data suggest that only during BSO treatment is there a R-lipoic acid-mediated increase in mitochondrial GSH to counter BSO generated ROS production.We were curious to know whether the effect of R-lipoic acid on GSH levels was due to an induction of g-GCL activity.Han et al.(1997)have shown that R-lipoic acid increases de novo synthesis of glutathione by improving cystine utilization.It is also possible that reduction of R-lipoic acid to dihydrolipo-ate in vivo might cause oxidation of GSH to GSSG in turn inducing GCL activity.However,since total glu-tathione estimations in our experiments involved quan-titation of both GSHþGSSG,depletion of GSH cannot be due to the accumulation of GSSG thus ruling out the possibility that increased GSSG concentration might be affecting the g-GCL activity.Fig.4shows that BSO treated cells exhibit$50%decrease in g-GCL activity compared to the untreated cells.Interestingly, cells pretreated with R-lipoic acid upon incubation with BSO showed an increase in g-GCL activity compared to cells treated with BSO alone.These data suggest that R-lipoic acid might contribute to an increased GSH pool during BSO treatment due to the induction of g-GCL activity.However,when cells are treated with R-lipoic acid alone there is a signifi-cant increase($1.6fold)in GSH levels without a concomitant increase in g-GCL activity suggesting that GSH levels are preserved by the direct anti-oxidant properties of R-lipoic acid and not due to increased g-GCL activity(Fig.2a).Decreases in mitochondrial NADH dehydrogenase(complex I)activity associated with GSH depletion also appear to be preserved via R-lipoic acid pretreatment(Fig.3).Taken together, these data suggest that GSH depletion,which may lead to oxidation of protein sulfhydryl residues in the mito-chondrial complex I important for normal functions484S.Bharath et al./NeuroToxicology23(2002)479–486resulting in profound effects on subsequent mitochon-drial performance,may be prevented by the direct action of R-lipoic acid.Our earlierfindings suggested that the activity of NADH dehydrogenase,the enzy-matic component of complex I,appears to be thiol-regulated(Jha et al.,2000).The preservation of mito-chondrial complex I activity via R-lipoic acid suggests that it protects against the oxidation of proteins by preventing the use of the cellular GSH pool or by increasing the de novo synthesis of cellular GSH in the presence of BSO-mediated oxidative stress.Whether such treatment would be effective in actually altering brain levels of GSH and thus providing beneficial effects in vivo has not yet been demonstrated. However,our data suggest that maintaining thiol homeostasis may be critical for protecting dopami-nergic neurons of the SN against neurodegeneration and that antioxidants such as R-lipoic acid may be of therapeutic value in PD.It would be of interest to conduct additional experiments using intermediates of dopamine metabolism or MPTP to explore thera-peutic value of R-lipoic acid pretreatment in PD. Nevertheless,since GSH depletion is the earliest event in PD pathogenesis,our data clearly suggests that R-lipoic acid can prevent the deleterious effects that follow by preventing mitochondrial GSH depletion.ACKNOWLEDGEMENTSThis work was supported by a grant from the National Institute of Health(NIH,R01AG12141) to JKA and by a grant from the Ellison Foundation (SS-0422-99),the National Institute of Health (NIH,R01,AG17140),and the National Institute of Environmental Health Sciences Center(NIH,P30, ES01896)to BNA.We thank Dr.M.Jyothi Kumar for technical help and criticaldiscussionsandDr.Simon Melov,Buck Institute,for use of his double beamed spectrophotometer.REFERENCESAdams Jr,JD,Chang ML,Klaidman L.Parkinson’s disease-redox mechanisms.Curr Med Chem2001;8:809–14.Ames BN.Micronutrients prevent cancer and aging.Toxicol Lett 1999;103:5–18.Andersen JK,Mo JQ,Hom DG,Lee FY,Harnish P,Hamill RW, McNeill TH.Effect of buthionine sulfoximine,a synthesis inhibitor of the antioxidant glutathione,on murine nigrostriatal neurons.J Neurochem1996;67:2164–71.Beal MF.Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses.Ann Neurol1992;31:119–30.Burke RE.Parkinson’s disease.In:Koliatos,Ratan RR,editors. Cell death and disease of the nervous system.Totowa(NJ): Humana Press,1998.p.459–75.Bushtamante J,Lodge JK,Marcocci L,Tritschler HJ,Packer L, Rihn BH.Alpha-lipoic acid in liver metabolism and disease. Free Radic Biol Med1998;24:1023–39.Davey GP,Peuchen S,Clark JB.Energy thresholds in brain mitochondria:potential involvement in neurodegeneration.J Biol Chem1998;273:12753–7.Fuchs J,Packer L,Zimmer G.Lipoic acid in health and disease. New York:Marcel Dekker,1997.Greene L,Tischler A.Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor.Proc Natl Acad Sci USA1976;73: 2424–8.Haas RH,Nasirian F,Nakano K,Ward D,Pay M,Hill R,Shults CW.Low platelet mitochondrial complex I and complex II/III activity in early untreated Parkinson’s disease.Ann Neurol 1995;37:714–22.Hagen TM,Ingersoll RT,Lykkesfeldt J,Liu J,Wehr CM,Vinarsky V,Barthlomew JC,Ames AB.(R)-alpha-lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage,and increased metabolic rate. FASEB J1999;13:411–8.Hagen TM,Vinarsky V,Wehr CM,Ames BN.(R)-alpha-lipoic acid reverses the age-associated increase in susceptibility of hepatocytes to tert-butylhydroperoxide both in vitro and in vivo. Antiox Redox Signal2000;2:473–83.Hager K,Marahrens A,Kenklies M,Riederer P,Munch G.Alpha-lipoic acid as a new treatment option for Alzheimer type dementia.Arch Gerontol Geriat2001;32:275–82.Hallman H,Lange J,Olson L,Stromberg I,Jonsson G. Neurochemical and histochemical characterization of neurotoxic effects of1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on brain catecholamine neurons in the mouse.J Neurochem1985;44: 117–27.Han D,Handelman G,Marcocci L,Sen CK,Roy S,Kobuchi H, Tritschler HJ,Flohe L,Packer L.Lipoic acid increases de novo synthesis of cellular glutathione by improving cystine utilization. Biofactors1997;6:321–38.Head KA.Natural therapies for ocular disorders,part two: cataracts and glaucoma.Alternative Med Rev2001;6:141–66. Hillered L,Chan PH.Effects of arachidonic acid on respiratory activities in isolated brain mitochondria.J Neurosci Res 1988;19:94–100.Huang CS,Chang LS,Anderson ME,Meister A.Catalytic and regulatory properties of the heavy subunit of rat kidney gamma-glutamylcysteine synthetase.J Biol Chem1993;268:19675–80. Jacob S,Henriksen EJ,Tritschler HJ,Augustin HJ,Dietz GJ. Improvement of insulin-stimulated glucose disposal in type2 diabetes after repeated parenteral administration of thioctic acid.Endocrinol Diabetes1996;104:284–8.Jenner P.Altered mitochondrial function,iron metabolism and glutathione levels in Parkinson’s disease.Acta Neurol Scand Suppl1993;146:6–13.Jha N,Andersen JK.Loss of glutathione(GSH)in Parkinson’s disease:how does GSH act to protect dopaminergic neurons of the substantia nigra?In:Pandalai SG,editor.Recent researchS.Bharath et al./NeuroToxicology23(2002)479–486485。

表面处理制程简介

表面处理制程简介
5. 無電解電鍍法(Electroless Method): 利用 化學反應之方式將金屬(尤其是銅、鎳)沉 積於塑膠物品上之方法。
九、彩色電鍍 製程:
IQC
Primer
Color Paint
PVD
UV Hard Coat
Shipping
FQC
100% Inspection
九、彩色電鍍 產品:
陽極: Me + XH2O → MeOX + 2XH+ + 2Xe- 陰極: H2O + e- → 1/2H 2+ OH-
八、EMI方法及應用
1.金屬漆料噴塗(Conductive coating):有許 多含有金、銅、鎳…等之導電漆料,利用傳 統之噴塗設備即可使用,然由於成形品愈來 愈具複雜性,均勻之噴塗為此法之一大問題, 另外亦會產生剝落。
E-Beam heating: The high voltage power supply provides 5 to 10KeV to accelerate the electrons from the filament to the evaporant. Most of kinetic energy of electrons is converted to heat on impingement .
六、物理氣相沉積 (Physical Vapor Deposition)
Evaporation
Reactive evaporation: Metal atoms are evaporated from an evaporant source with a partial pressure of a reactive gas present in the chamber.

电气工程及其自动化专业英语词汇

电气工程及其自动化专业英语词汇

电气工程及其自动化Electrical Engineering and Automation专业英语词汇English VocabularyEdit by zhao Guoshu,on Aprial 7,2009电气工程专业英语词汇表electrical engineering 电气工程generator发电机gas insulated substation GIS 气体绝缘变电站turbogenerator 汽轮发电机neutral point中性点hydrogenerator 水轮发电机movable contact 动触头hydraulic turbine 水轮机fixed contact静触头steam turbine 汽轮机arc-extinguishing chamber灭弧室arc-extinguish 灭弧arc-suppression 灭弧setting value整定值dynamo直流发电机inductive (capacitive)电感的(电容的) capacitive coupling电容性耦合inductive coupling电感性耦合stray capacitance杂散电容grounding capacitance 对地电容power capacitor 电力电容residual capacitance 残余电容capacitor bank 电容器组coupling capacitor耦合电容parasitic coupling capacitor寄生耦合电容decoupling capacitor 去耦电容bypass capacitor 旁路电容motor 电动机stray inductance 杂散电感distributed inductane分布电感stator定子sphere gap 球隙rotor转子bushing tap grounding wire 套管末屏接地线power transformer电力变压器electrostatic voltmeter 静电电压表multimeter万用表voltage drop电压降forward voltage drop正向压降variable transformer 调压变压器power transfer电能传输,功率转换ammeter电流表taped transformer 多级变压器step up (down) transformer升(降)压变压器voltage divider 分压器circuit breaker (CB) 断路器chopper 斩波器over current过电流surge impedance 波阻抗match the impedance 阻抗匹配neutral point中性点dead tank oil circuit breaker 多油断路器schering bridge 西林电桥live tank oil circuit breaker 油断路器rogowski coil !"#$%线英vacuum circuit breaker'(断路器oscilloscope)波器sulphur hexafluoride breaker SF6断路器peak voltmeter *值电压表trip unit +,器potential transformer PT 电压体感器conductor .线current transformer CT 电流体感器cascade transformer /级变压器disconnector 0123earthing switch 接地汽轮test object 456synchronous generator78发电机synchronous motor/machine78电动机stepper/stepping motor89电机brushless DC motor:;直流电机form factor波灭弧室gain?@analog AB的digital>C的linear power supply工感电的steady-state FGon-state voltage HG压降on-state resistance HG电阻detection impedance IJ阻抗asynchronous machine K8电机substation 变电站insulator 绝缘子hydro power station 水力发电站lightning arrester LM器thermal power station N力发电站电气工程专业英语词汇表metal oxide arrester MOA OPQLM器nuclear power station R电站bus bar S线oil-filled power cable T油电力电旁overhead line V(线mixed divider (阻容)W合分压器transmission line 传输线XLPE cable XYZ[\电旁(coaxial) cable (7])电旁relay^电器contactor接触器pull-in current 动末电流drop-out current`a电流Schmitt trigger bcd触发器iron core eftuned circuit 调正电路interface circuit接向电路integrated circuit (IC)ij电路winding k组suspension insulator lm绝缘子bushing 套管time-varying n变的porcelain insulator op绝缘子front(tail) resistance 波头(q)电阻glass insulator rs绝缘子inverter station 换流站flash counter M电断室器steel-reinforced aluminum conductorufvw线charging(damping) resistor T电(阻阻)电阻tank y体point plane gap z{|隙earth(ground) wire 接地线exciting winding}~k组grading ring •压环trigger electrode 触发电极firing angle触发角highvoltage engineering 高电压工程glow discharge 辉光放电highvoltage testing technology 高电压性验技术harmonic g波fundamental%波power electronics 电力电子microelectrics technology微电子技术automatic control自动控制principles of electric circuits电路原理digital signal processing>C信号处理digital signal processor>C信号处理器power system 电力弧统impulse current冲击电流power network电力网络impulse flashover 冲击闪络insulation绝缘positive feedback正反馈negative feedback负反馈inhomogenous field 不晶匀场overvoltage过电压transient voltage 瞬强电压clamp voltage箝位电压insulation coordination 绝缘配合aging老寿internal discharge 内部放电direct current (DC)直流电alternating current (AC)X流电lightning stroke M电波AC transmission system X流输电弧统lightning overvoltage M电过电压plug 插头socket插座arc discharge电弧放电dielectric strength 绝缘强度reliability"靠性maintainability维修性durability耐久性validity有效性longevity寿命electric leakage switch漏电汽轮loss angle (介质)损耗角attachment coefficient 附着匀场magnetic field~场permeability~.率attenuation factor 衰减匀场mean free path 平晶自由程anode (cathode)阳极(阴极)mean molecular velocity 平晶分子速度breakdown (电)击穿negative ions 负号子电气工程专业英语词汇表bubble breakdown 气泡击穿non-destructive testing 非破坏性性验cathode ray oscilloscope 阴极射线汇波器non-uniform field 不晶匀场cavity (穴,腔partial discharge局部放电corona 电晕peak reverse voltage 反向表值电压critical breakdown voltage 临界击穿电压withstand voltage 耐受电压phase-to-phase voltage 相电压switching overvoltage ('(23的)操阳过电压recovery voltage 恢复电压voltage rating额定电压blocking voltage 截止电压reverse-blocking voltage 反向截止电压threshold voltage 阈值电压saturation voltage 饱和电压breakdown voltage击穿电压composite insulation 组合绝缘photoelectric emission 光电发射photon 光子optocoulper光耦solar photovoltatic array 太阳能光伏阵列optical fiber 光学纤维light-activated SCR光控晶闸管snubber curcuit缓冲电路holding current维持电流discharge 放电dielectric电介质,绝缘体polarity effect极性效应dielectric constant 介质常矩dielectric loss 介质损耗quasi-uniform field 稍不晶匀场radio interference :线干扰divider ratio 分压器分压比rating of equipment 设备额定值grounding接地routing testing 常规脂验electric field 电场electrochemical deterioration 电器学腐蚀shielding 屏蔽electron avalanche 电子崩short-circuit test短路性验no-load test(载脂验normally-open常闭normally-closed常闭electronegative gas 电负性气体space charge (|电荷epoxy resin 环效树脂streamer breakdown 流注击穿expulsion gap 灭弧油隙surface breakdown 表面击穿field strength场强sustained discharge 自持放电field stress 电场力field distortion 场畸变thermal breakdown 热击穿field gradient 场梯度treeing 树枝放电field emission 场致发射uniform field •匀场flashover 闪络wave front(tail) 波头(恢)gaseous insulation 气体绝缘prime mover原动机power factor功率因矩torque力矩,转矩periphery 外围distribution automation system配电网自动器弧统distribution system配电弧统distribution feeder配电线路servomechanism伺服机构(=统)servo system伺服因统automatic meter reading 自动抄表frequency changer D率变换器boiler 锅炉armature winding 电枢停组field winding励轻停组internal combustion engine 内燃机brush 电静deenergize 断电commutator换向器carbon brush碳枝underground cable 地下电旁EMF(Electro-Motive force) 电动势电气工程专业英语词汇表counter EMF反电动势MMF(Magneto-Motive Force)~动势flux linkage~Yreluctance~阻loop system 环网匀统demagnetization 退轻,去林relay panel ^电器屏trip circuit跳闸电路tertiary winding 第三停组switchboard 配电盘,汽轮屏eddy current涡流instrument transducer J量蚀感器copper loss铜损oil-impregnated paper 油浸纸绝缘iron loss e损bare conductor 裸蔽线leakage flux漏纤度flux-density ~Hc度reclosing 重合闸autotransformer 自耦变压器distribution dispatch center 配电调度中心Zero sequence current 零序电流pulverizer 磨煤机series (shunt) compensation /(并)联补偿drum 汽包,炉筒restriking 电弧重燃superheater 过热器automatic oscillograph 自动录波仪peak-load *荷tidal current 潮流prime grid substation 主网变电站trip coil 跳闸线英instantaneous power 瞬强功率active power有功功率reactive power:功功率radian frequency角部率current capacity载流容量synchronous condenser 78调相机active power有功功率main and transfer busbar 单量线带旁路shunt reactor 并联电抗器feeder 馈电线blackout 断电、停电skin effect i肤效应extra-high voltage (EHV) 超高压potential stress 电位应力(电场强度)ultra-high voltage (UHV) d高压domestic load 民用电crusher 碎煤机reserve capacity 备用容量fossil-fired power plant N电厂baghouse i尘室combustion turbine 燃气轮机stationary (moving) blade 固定(角动)叶片right-of-way 线路走廊shaft转套rectifier整流器full-wave rectification 全波整流forward-biased 正向偏置ripple脉动spike 尖备kinetic(potential) energy 动(势)能pumped storage power station 抽水蓄能电站reactance (impedance) 电抗(阻抗)reactor 电抗器light(boiling)-water reactor 轻(沸)水反应堆reactive 电抗的,头功的stator(rotor) 定(转)子phase displacement (shift) 相移armature 电枢surge 冲击,过电压salient-pole凸极retaining ring 护环slip ring滑环collector ring i电环carbon brush炭千arc suppression coil 消弧线英short-circuit ratio短路比cross section横截面primary(backup) relaying 主(后备)^电保护induction感应phase shifter 移相器sinusoidal distribution 正弦分布autotransformer 自藕变压器power line carrier (PLC) 电力线载波(器) bushing 套管line trap 线路限波器turn (turn ratio)匝(匝比,变比)电气工程专业英语词汇表uninterruptible power supply(UPS)不列断电的switch-mode/switching power supply23电的power factor功率因矩line-frequency 工感spot power price 实湿电价tap 分接头time-of-use(tariff) 分功(电价)XLPE(Cross Linked Polyethylene)X联零序磨(电旁)arc re-ignition电弧重燃rms (root mean square) •方根值operation mechanism 操动机构RF (radio frequency) 射部pneumatic(hydraulic) 气动(液压)rpm (revolution per minute) 转/分nameplate 铭牌LAN (local area network) 局域网independent pole operation 分相操阳LED (light emitting diode)发光二极管photo transisitor 光电三极管free-wheeling diode续流二极管schottky barrier diode肖委炭势垒二极管fast-recovery diode快恢复二极管kilovolt千伏kiloampere 千安millisecond 毫秒microsecond微秒malfunction 失灵single (dual, ring) bus 单(双,环不)S线shield wire LM线IC (integrated circuit)ij电路creep distance 爬电距根FFT (fast Fourier transform) 快速傅立叶变换silicon rubber 硅橡胶telemeter 遥甩composite insulator 合能绝缘子load shedding 甩负荷invertion 逆变oscillator 晶体振荡器converter (inverter) 换流器(逆变器)step-down converter降压变换器step-up converter 升压变换器full-bridge converter全桥变换器PWM(pulse-width modulation)脉宽调制duty ratio 占后比soft-start软启动lateral 支线bus tie breaker S联断路器power-flow current 工感续流protective relaying^电保护sparkover 放电transfer switching 倒闸操阳silicon carbide碳三硅outgoing (incoming) line 出(9)线Zinc oxide OPQphase lead(lag) 相位超前(滞后)withstand test 耐压性验static var compensation (SVC) 静止馈功补偿dispatcher 调度员Flexible AC transmission system (FACTS)灵活活流输电弧统supervisory control and data acquisition (SCADA) 监控与秒据采校EMI (electromagnetic interference)电林干扰EMC (electromagnetic compatibility)电林兼容ISO (international standardization organization) 国际标准软组织GIS (gas insulated substation, geographic information system)气体绝缘变电站,地理信息毫统IEC (international Electrotechnical Commission)国际电工(技术)委员会IEEE (Institute of Electrical and Electronic Engineers)电气与电子工程师学会(美)IEE (Institution of Electrical Engineers)电气工程师学会(英)scale 刻度,量程calibrate 校准rated 额定的terminal接线端子fuse 熔断器,保险丝,熔丝humidity湿度resonance g振,共振moisture潮湿,湿气analytical 解析的电气工程专业英语词汇表numerical>C的amplitude modulation (AM)调幅frequency-domain D域frequency modulation (FM)调感time-domain n域binary二垒制operation amplifier运算放大器octal八垒制filter滤波,滤波器active filter有插滤波器decimal十垒制passive filter :E滤波器hexadecimal 十六垒制rms(root mean square)•方根。

甲强龙结合多索茶碱方案对AECOPD患者肺通气功能及血清炎性因子表达的影响

甲强龙结合多索茶碱方案对AECOPD患者肺通气功能及血清炎性因子表达的影响

生命科学仪器 2023年第21卷/第5期技术与应用79作者简介:章昱(1987 ),男,汉族 ,江苏如皋市人,本科,住院医师,研究方向:内科,邮箱:604461893@q q.c o m ㊂甲强龙结合多索茶碱方案对A E C O P D 患者肺通气功能及血清炎性因子表达的影响章 昱 张晨雨(如皋市中医院急诊内科,江苏如皋226500)摘要 目的探讨甲强龙结合多索茶碱方案对慢性阻塞性肺疾病急性加重期(A E C O P D )患者的治疗效果㊂方法将110例A E C O P D 患者按随机双盲法分为两组,对所有患者进行相同的基础治疗方案时,对照组采用多索茶碱治疗,观察组在对照组相同的治疗方案上采用甲强龙治疗;对比两组治疗前后肺通气功能㊁血清炎症表达等㊂结果治疗1周后:观察组的肺通气功能高于对照组,血清超敏C 反应蛋白(h s -C R P )㊁白细胞介素(I L )-17㊁基质金属蛋白酶-9(MM P -9)表达低于对照组,而血氧分析改善程度高于对照组(P <0.05);观察组C O P D 评估测试(C A T )评分(15.43ʃ2.48)分低于对照组的(21.73ʃ3.34)分,差异明显(P<0.05)㊂两组治疗不良反应发生情况比较(P>0.05)㊂两组出院后3个月未因C O P D 急性发作而住院治疗,无复发情况㊂结论甲强龙结合多索茶碱可明显改善A E C O P D 患者肺通气功能,降低血清炎性因子表达,值得临床应用㊂关键词 甲强龙;多索茶碱;慢性阻塞性肺疾病急性加重期E f f e c t o f m e t h y l a n k y o n e c o m b i n e d w i t h d o s o t h e l l i n e r e g i m e n o n p u l m o n a r y v e n t i l a t o r yf u n c t i o n a n d e x p r e s s i o n o f s e r u m i n f l a m m a t o r y fa c t o r s i n A E C O P D p a t i e n t s Z h a n g Y u a n d Z h a n g C h e n yu (R u g a o H o s p i t a l o f T r a d i t i o n a l C h i n e s e M e d i c i n e ,R u g a o ,J i a n gs u 226500)ʌA b s t r a c t ɔO b je c t i v e :t o e v a l u a t e t h e ef f i c a c y o f m e t h y l p r e d n i s o l o n e c o m b i n e d w i t h d o x o f y l l i n e i n t h e t r e a t m e n t o f a -c u t e e x a c e r b a t i o n o f c h r o n i c o b s t r u c t i v e p u l m o n a r y di s e a s e (A E C O P D ).M e t h o d s :110A E C O P D p a t i e n t s w e r e r a n d o m l y d i v i d e d i n t o t w o g r o u p s u s i n g a d o u b l e -b l i n d m e t h o d ,,t h e o b s e r v a t i o n g r o u p w a s t r e a t e d w i t h m e t h yl -p r e d n i s o l o n e i n t h e s a m e t r e a t m e n t p l a n a s t h e c o n t r o l g r o u p ,a n d t h e p u l m o n a r y ve n t i l a t i o nf u n c t i o n a n d s e r u m i n -f l a mm a t o r y e x p r e s s i o n w e r e c o m p a r e d b e t w e e n t h e t w og r o u ps b e f o r e a n d a f t e r t r e a t m e n t .R e s u l t s :a f t e r o n e w e e k o f t r e a t m e n t ,t h e p u l m o n a r y v e n t i l a t i o n f u n c t i o n i n t h e o b s e r v a t i o n g r o u p w a s h i g h e r t h a n t h a t i n t h e c o n t r o l g r o u p,a n d t h e s e r u m l e v e l s o f h s -C R P ,I L -17a n d Mm p -9i n t h e o b s e r v a t i o n g r o u p we r e l o w e r t h a n t h o s e i n t h e c o n -t r o l g r o u p ,w h i l e t h e s e r u m l e v e l s of h s -C R P ,I L-17a n d MM P-9i n t h e i n t e r l e u k i ng r o u p we r e l o w e r t h a n t h o s e i n t h e c o n t r o l g r o u p ,t h e i m p r o v e m e n t d e g r e e of b l o o d o x yg e n a n a l y s i s w a shi gh e r t h a n t h a t o f t h e c o n t r o l g r o u p (p <0.05),a n d t h e s c o r e o f C O P D a s s e s s m e n t (C a t )i n t h e O b s e r v a t i o n G r o u p (15.43ʃ2.48)w a s l o w e r t h a n t h a t o f t h e c o n t r o l g r o u p (21.73.34),t h e d i f f e r e n c e w a s s i g n i f i c a n t (p <0.05).T h e i n c i d e n c e o f a d v e r s e r e a c t i o n s i n t w o g r o u p s w a s c o m p a r e d (P >0.05).T w o g r o u p s w e r e d i s c h a r g e d w i t h o u t h o s pi t a l i z a t i o n f o r a c u t e e x a c e r b a t i o n o f C O P D w i t h i n 3m o n t h s ,a n d t h e r e w a s n o r e c u r r e n c e .C o n c l u s i o n :m e t h y l pr e d n i s o l o n e c o m b i n e d w i t h d o x o f y l l i n e c a n i m p r o v e p u l m o n a r y v e n t i l a t i o n f u n c t i o n a n d d e c r e a s e t h e e x p r e s s i o n o f s e r u m i n f l a mm a t o r yf a c t o r s i n p a t i e n t s w i t h A E C O P D ,w h i c h i s w o r t h y o f c l i n i c a l a p pl i c a t i o n .ʌK e y wo r d s ɔm e t h y l p r e d n i s o l o n e ;d o x o f y l l i n e ;a c u t e e x a c e r b a t i o n o f c h r o n i c o b s t r u c t i v e p u l m o n a r y d i s e a s e 中图分类号:R 322.3+5 文献标识码:A D O I :10.11967/2023211016慢性阻塞性肺疾病(c h r o n i c o b s t r u c t i v e p u l -m o n a r y di s e a s e ,C O P D )是由气道炎症诱导所致,随着疾病进展,当疾病进入急性加重期时,胸闷㊁气短等症状持续恶化㊁加重,痰液增多,并伴发热㊁乏力等症状,明显危及患者生命安全[1]㊂对慢性阻塞性肺疾病急性加重期(A c u t e e x a c e r b a t i o np h a s e o f c h r o n i c o b s t r u c t i v e p u l m o n a r y di s e a s e ,A E C O P D )的治疗,主要是从氧疗㊁降炎㊁控制感染㊁支气管扩张等方面进行处理[2]㊂其中多索茶碱是一种甲基黄嘌呤衍生物,可直接作用于支气管平滑肌,起到抗炎㊁扩张支气管的作用[3]㊂然而,A E C O P D 发病机制复杂,临床多需要结合其技术与应用生命科学仪器 2023年第21卷/第5期80他药物共同治疗,方能提高临床治疗效果㊂甲强龙是一种短效的糖皮质激素,具有抗炎㊁抗免疫等作用,多作为危急以及紧急病症的首选药物[4]㊂但甲强龙对A E C O P D 的治疗情况,临床鲜有报道,尤其是甲强龙结合多索茶碱治疗效果及作用机制,临床报道较少,故而证实了该研究的可行性㊂基于此,现研究以A E C O P D 患者为例,对其采用甲强龙结合多索茶碱治疗,对其效果报道如下㊂1 资料与方法1.1 临床资料 使用G p o w e r 软件进行样本量计算,将E f f e c t s i z e 设为0.2,I 型错误的概率为0.05,检验效能设为0.95,计算样本量,再考虑15%~20%的失访率,最终确定样本量110例数㊂110例A E C O P D 患者均于2021年1月-2022年12月到院就诊㊂按随机双盲法分为两组,对照组55例,男31例,女24例;年龄为45~80(61.89ʃ5.82)岁;C O P D 病程:3~18(9.92ʃ3.14)年;吸烟史16例;A E C O P D 分级:I 级12例,Ⅱ级26例,Ⅲ级17例;基础疾病:高血压/糖尿病/冠心病/无分别为16/12/8/19例;观察组55例,男28例,女27例;年龄为45~82(62.17ʃ5.96)岁;C O P D 病程:3~20(10.14ʃ3.20)年;吸烟史19例;A E C O P D 分级:I 级10例,Ⅱ级25例,Ⅲ级20例;基础疾病:高血压/糖尿病/冠心病/无分别为18/15/8/14例;两组的临床资料经统计比较(P>0.05),可对比㊂本研究符合医院医学伦理委员会审批标准,并审核通过㊂1.2 纳排条件纳入条件:(1)患者经临床表现㊁血氧㊁实验指标等综合检查,符合A E C O P D 标准[5];(2)患者疾病发作处于急性期;(3)近4周有糖皮质激素㊁茶碱类药物等治疗史;(4)对研究具体细则知晓,签署了同意书㊂排除条件:(1)伴肺结核㊁哮喘㊁肺结节㊁肺恶性肿瘤等其他肺部疾病者;(2)伴呼吸衰竭㊁心力衰竭㊁肝肾不全等疾病者;(3)有长期药物依赖史者;(4)对研究内的药物存在过敏现象;(5)血糖控制不佳㊁出血㊁溃疡活动期等对激素有禁忌症者㊂1.3 方法 所有患者在入院后均进行吸氧㊁祛痰㊁补液等基础治疗,并进行抗炎㊁纠正酸碱平衡㊁平喘㊁止咳,针对基础疾病进行降压㊁降糖等治疗㊂对照组:多索茶碱(宁波市天衡制药,国药准字H 20000075),剂量为250m g,添加于葡萄糖溶液250m L ,静脉滴注,每天1次,连续1周;观察组:多索茶碱的用法㊁用量同对照组,甲强龙(天津金耀药业,国药准字H 20123319),40m g 添加生理盐水100m L 稀释后,缓慢注射,1天1次,连续1周㊂1.4 观察指标1.4.1 在治疗前㊁治疗1周后即进行以下相关指标检测:(1)肺通气功能:北京西化仪科技有限公司产的肺功能检测仪检测,包括第一秒用力呼气容积占预计值的比率(F o r c e d e x p i r a t o r y vo l -u m e i n o n e s e c o n d %,F E V 1%)㊁最大自主通气量(m a x i m a l v o l u n t a r y v e n t i l a t i o n ,MV V )㊁用力肺活量(f o r c e d v i t a l c a p a c i t y,F V C );(2)血清炎症表达:采集患者空腹状态时的静脉血3m L ,先进行离心处理,时间为10m i n ,转速为每分钟3000r ,将离心后提取的血清样本用酶联免疫法检测,指标有超敏C 反应蛋白(H y pe r s e n s i t i v e C -r e a c t i v e pr o t e i n ,h s -C R P )㊁白细胞介素(i n t e r l e u k i n ,I L )-17㊁基质金属蛋白酶-9(m a t r i x m e t a l l o pr -o t e i n a s e -9,MM P-9);(3)血气分析:取患者的股动脉血4m L ,用美国西门子产的血气分析仪测定动脉血氧分压(a r t e r i a l p a r t i a l p r e s s u r e o f o x y-g e n ,P a O 2)㊁血二氧化碳分压(P a r t i a l P r e s s u r e o f C a r b o n D i o x i d e ,P a C O 2)以及氧合指数(O I );(4)临床症状:即采用C O P D 评估测试(C O P D A s -s e s s m e n t T e s t ,C A T )评分[6],量表主要是评估患者出现的咳嗽㊁咳痰㊁运动㊁睡眠㊁胸闷等症状,共8项标准,总分在8~40分,分值随病情程度的加重而增加㊂1.4.2 不良反应评价:即观察患者在整个1周的治疗过程中,根据患者用药的说明书情况,观察是否出现与其相符的不良反应㊂1.4.3 记录患者出院3个月后的疾病复发率㊂1.5 统计学方法 S P S S 26.0统计学软件处理相关数据㊂计量数据符合正态分布,以(x ʃs )表示,组间㊁组内分别用独立㊁配对样本t 检验;计数资料以率(%)表示,采取2检验;P<0.05为差异有统计学意义㊂2 结果2.1 肺通气功能 治疗前:组间检测时的肺功能比较(P >0.05);治疗后:组内㊁组间指标差异值明显(P <0.05),见表1㊂2.2 血清炎症表达 治疗前:组间检测时的各项指标表达值比较(P >0.05);治疗后:组内㊁组间指生命科学仪器 2023年第21卷/第5期技术与应用81标差异值明显(P <0.05),见表2㊂2.3 血气分析 治疗前:组间检测时的血气分析指标比较(P >0.05);治疗后:组内㊁组间指标差异值明显(P <0.05),见表3㊂表1 两组肺通气功能比较(x ʃs)组别F E V 1%(%)F V C (L )MV V (L /m i n)治疗前治疗后治疗前治疗后治疗前治疗后观察组(n =55)45.83ʃ5.8171.48ʃ6.92a 2.08ʃ0.413.13ʃ0.52a 84.83ʃ6.28151.45ʃ8.24a 对照组(n =55)46.18ʃ5.9665.73ʃ5.84a2.11ʃ0.432.76ʃ0.48a85.17ʃ6.34136.73ʃ6.64at 0.3124.7090.3743.8770.28310.316P0.756<0.0010.709<0.0010.778<0.001注:与相同指标同组的治疗前相比,aP <0.05表2 两组检测指标炎症表达比较(x ʃs)组别h s -C R P (m g/L )I L -17(n g/L )MM P -9(n g/m L )治疗前治疗后治疗前治疗后治疗前治疗后观察组(n =55)26.13ʃ3.866.49ʃ1.24a 241.04ʃ35.58121.26ʃ12.08a 0.80ʃ0.140.32ʃ0.12a 对照组(n =55)25.87ʃ3.938.92ʃ1.36a238.89ʃ34.19152.84ʃ13.65a0.78ʃ0.160.48ʃ0.13at 0.3509.7920.32312.8490.6986.707P0.727<0.0010.747<0.0010.487<0.001 注:与相同指标同组的治疗前相比,aP <0.05表3 两组血气分析指标比较(m m H g,x ʃs )组别P a O 2P a C O 2O I治疗前治疗后治疗前治疗后治疗前治疗后观察组(n =55)45.83ʃ6.3675.84ʃ5.86a 81.13ʃ8.3656.28ʃ6.40a 218.83ʃ35.46389.83ʃ46.28a 对照组(n =55)46.17ʃ6.4269.83ʃ5.73a79.89ʃ8.4362.83ʃ6.52a222.13ʃ36.84342.18ʃ45.08at 0.2795.4380.7755.3170.4795.470P0.781<0.0010.440<0.0010.633<0.001 注:与相同指标同组的治疗前相比,aP <0.052.4 C A T 评分 治疗前:组间症状评分比较(P>0.05);治疗后:组内㊁组间症状评分明显(P<0.05),见表4㊂表4 组间症状评分比较(分,x ʃs)组别治疗前治疗后tP观察组(n =55)61.06ʃ6.3515.43ʃ2.4849.640<0.001对照组(n =55)58.96ʃ8.1621.73ʃ3.3431.315<0.001t 1.50611.231P0.135<0.0012.5 不良反应 观察组1例恶心,1例头痛,2例心悸,1例失眠,发生率9.09%;对照组1例恶心,1例失眠,发生率3.64%;差异不明显(2=0.610,P =0.435)㊂2.6 疾病复发率 两组出院后3个月未因C O PD 急性发作而住院治疗,无复发情况㊂3 讨论C O PD 是一种因气道重构造成气道进行性阻塞及不完全可逆性气流受限的肺部疾病,患者多出现反复㊁日趋加重的咳嗽㊁气促㊁喘息等症状㊂感染是A E C O P D 最主要诱因,临床治疗时,需要考虑患者短期目标,即在短时间内治愈或改善患者临床症状,恢复肺功能,减轻支气管炎症反应[7]㊂多索茶碱是促进气道扩张,改善患者肺通气功能的主要药物,药效高于传统茶碱类药物,且起效迅速,作用持久,已在临床广泛应用[8]㊂但对气道高炎症反应,临床多要联合其他药物共同治疗㊂甲强龙是一种中效糖皮质激素,由人工合成,肺组织渗透性强,对肾上腺垂体系统影响较低,生物半衰期短,不易在体内蓄积,用药安全性高,对炎症性疾病及免疫性疾病有显著效果[9]㊂本研究发现,治疗1周后:观察组的肺通气功能高于对照组,C O P D 评估测试(C A T )评分(15.43ʃ2.48)分低于对照组的(21.73ʃ3.34)分,血氧分析改善程度高于对照组(P <0.05)㊂其结果表明,甲强龙结合多索茶碱能提高患者肺通气功能,减轻呼吸困难症状㊂张逍等[10]学者对A E C O P D 合并呼吸衰竭患者采用呼吸机治疗时结合甲强龙,结果显示患者肺功能明显提高,呼吸力学显著改善㊂各研究证实了甲强龙联合应用的优越性,但对其研究较少,故而证实了该研究的创新性㊂多索茶碱是一种新型黄嘌呤衍生物,用药技术与应用生命科学仪器 2023年第21卷/第5期8230m i n 即可达到治疗效果,作用持续12h 左右,通过对磷酸二酯酶活性的抑制,可降低支气管平滑肌的收缩能力,进而舒张患者支气管,降低气道高反应,改善患者肺通气功能,纠正患者缺氧状态[11]㊂甲强龙是一种合成的糖皮质激素,可轻易渗透至细胞膜,并有效结合胞浆内特异性受体,起到显著的抗炎㊁免疫抑制及抗过敏活性等作用,以此能降低气道高炎症反应,改善患者肺通气功能[12]㊂炎症刺激是C O P D 急性加重的主要病理因子,高气道炎症反应会持续释放各种炎症介质及炎症细胞因子,当致炎因子持续损伤肺组织,使血管通透性增加,导致气道痉挛,造成C O P D 急性发作,导致患者肺功能持续恶化[13]㊂h s -C R P 是反映机体炎症程度的重要指标,其水平越高,气道炎症反应更加明显;MM P-9是一种脊柱基质金属蛋白酶,通过对细胞外基质的降解重塑,从而能维持细胞内外的动态平衡性;同时可分解呼吸道及肺内的复合物,参与到呼吸道重建的过程;另外通过调控其他细胞因子活性,导致肺内弹性酶活性异常,促进C O P D 的发生㊁进展;I L-17是诱导机体炎症反应的启动因子,可促进前炎性细胞的释放,增加机体炎症反应;同时可促进I L -6㊁肿瘤坏死因子(T N F )-α的分泌,以此促进气道平滑肌增生,导致患者气道重塑,加重病情程度[14]㊂研究显示,观察组在治疗后上述炎症因子表达低于对照组㊂多索茶碱作为支气管扩张剂,在舒张支气管的同时,可抑制炎症因子释放,缓解气道高炎症程度;甲强龙可促进淋巴细胞产生,激活淋巴细胞功能,抑制炎症细胞因子的花生,阻断花生四烯酸代谢产物的分泌途径,进而发挥显著的抗炎作用;另外甲强龙通过促进酶蛋白合成,发挥抗炎功效㊂因此两药联合能发挥显著的抗炎功效,抑制疾病病理因子,减轻疾病严重程度㊂而两组治疗不良反应发生情况以及出院后3个月的疾病复发率比较无差异,可能是两组用药仅1周时间,且样本量少,使近期及远期研究结果存在偏倚,故需要临床进一步探讨㊂综上所述,甲强龙结合多索茶碱可明显改善A E C O P D 患者肺通气功能,改善血气分析,降低血清炎性因子表达,且未增加治疗副作用,值得临床应用㊂但本研究尚有不足,研究样本量少,用药时间短,研究时间短,使研究结果存在偏颇,故需要未来研究扩大样本量㊁延长随访时间,从而为A E C O P D 的治疗提供新的研究方向㊂参考文献[1]M a c L e o d M ,P a pi A ,C o n t o l i M ,e t a l .C h r o n i c o b s t r u c t i v e p u l m o n a r y d i s e a s e e x a c e r b a t i o n f u n d a m e n t a l s :D i a gn o s i s ,t r e a t m e n t ,p r e v e n t i o n a n d d i s e a s e i m p a c t [J ].R e s p i r o l o g y ,2021,26(6):532-551.[2]M a t h i o u d a k i s A G ,J a n s s e n s W ,S i v a pa l a n P ,e t a l .A c u t e e x -a c e rb a t i o n s o fc h r o n i c o b s t r u c t i v e p u l m o n a r y di s e a s e :i n s e a r c h o f d i a gn o s t i c b i o m a r k e r s a n d t r e a t a b l e t r a i t s [J ].T h o -r a x ,2020,75(6):520-527.[3]李炜,王晓焰,马源,等.多索茶碱联合雾化吸入布地奈德㊁异丙托溴铵治疗慢性阻塞性肺疾病急性加重患者疗效研究[J ].创伤与急危重病医学,2022,10(6):442-445,452.[4]连换杰,刘玉娇,邓娅君.重组人干扰素α2b 联合甲强龙对喘息性支气管炎患儿E O S ㊁S P-D ㊁25-(O H )D 3水平的影响[J ].国际检验医学杂志,2022,43(12):1444-1447.[5]国家卫生健康委员会急诊医学质控中心,中华医学会急诊医学分会,中国医师协会急诊医师分会,等.中国慢性阻塞性肺疾病急性加重中西医诊治专家共识(2021)[J ].中华危重病急救医学,2021,33(11):1281-1290.[6]S t a n f o r d R H ,T a b b e r e r M ,K o s i n s k i M ,e t a l .A s s e s s m e n t o ft h e C O P D A s s e s s m e n t T e s t W i t h i n U.S .P r i m a r y C a r e [J ].C h r o n i c O b s t r P u l m D i s ,2020,7(1):26-37.[7]B a q d u n e s MW ,L e a p J ,Y o u n g M ,e t a l .A c u t e E x a c e r b a t i o n of C h r o n i c O b s t r u c t i v e P u l m o n a r y D i s e a s e [J ].C r i t C a r e N u r s Q ,2021,44(1):74-90.[8]金妍,石志华,周晓静,等.布地奈德混悬液联合多索茶碱对慢性阻塞性肺疾病患者疗效㊁肺功能及血气分析的影响[J ].解放军医药杂志,2021,33(3):63-67.[9]孟利青,方慧英,王金范.小剂量甲强龙治疗难治性支原体感染的临床疗效及对肺功能的影响[J ].中国妇幼保健,2020,35(20):3803-3805.[10]张逍,张传红.甲强龙联合B i P A P 呼吸机治疗A E C O P D 合并呼吸衰竭患者的疗效[J ].川北医学院学报,2022,37(11):1472-1475.[11]郑宇静,李婷,郭思瑞,等.多索茶碱与茶碱/氨茶碱治疗支气管哮喘和慢性阻塞性肺疾病的快速卫生技术评估[J ].中国药业,2023,32(12):112-115.[12]王谦.特布他林联合甲强龙治疗对慢性阻塞性肺病患者肺功能㊁血气分析及炎症因子的影响[J ].实用心脑肺血管病杂志,2018,26(z 1):90-91.[13]胡传玺,刘灵燕,李漫.血清白细胞介素-10㊁白细胞介素17㊁白细胞介素-23检测对慢性阻塞性肺疾病合并侵袭性肺曲霉菌感染的诊断及预后评估价值[J ].陕西医学杂志,2023,52(10):1415-1418.[14]宋伟伟,常双喜,禹彩霞,等.慢性阻塞性肺疾病合并肺部感染者T h 17/T r e g㊁I L -17水平与肺功能及C A T 评分的关系[J ].中国老年学杂志,2022,42(8):1843-1846.。

电气工程及其自动化专业英语

电气工程及其自动化专业英语
hydrogenerator 水轮发电机 moving contact 动触头 hydraulic turbine 水轮机 fixed contact 静触头 steam turbine 汽轮机 arc-extinguishing chamber 灭弧室 dynamo 直流发电机 stray capacitance 杂散电容 motor 电动机 stray inductance 杂散电感 stator 定子 sphere gap 球隙 rotor 转子 bushing tap grounding wire 套管末屏接地线 power transformer 电力变压器 electrostatic voltmeter 静电电压表 variable transformer 调压变压器 ammeter 电流表 taped transformer 多级变压器 grounding capacitance 对地电容 step up (down) transformer 升(降)压变压器 voltage divider 分压器 降 压变压器 circuit breaker CB 断路器 surge impedance 波阻抗 dead tank oil circuit breaker 多油断路器 Schering bridge 西林电桥 live tank oil circuit breaker 少油断路器 Rogowski coil 罗可夫斯基线圈 vacuum circuit breaker 真空断路器 oscilloscope 示波器 sulphur hexafluoride breaker SF6 断路器 peak voltmeter 峰值电压表 峰值电压表 potential transformer PT 电压互感器 conductor 导线 current transformer CT 电流互感器 cascade transformer 串级变压器 disconnector 隔离开关 coupling capacitor 耦合电容 earthing switch 接地开关 test object 被试品 synchronous generator 同步发电机 detection impedance 检测阻抗 asynchronous machine 异步电机 substation 变电站 Insulator 绝缘子 hydro power station 水力发电站 lightning arrester 避雷器 thermal power station 火力发电站 metal oxide arrester MOA 氧化锌避雷器 nuclear power station 核电站 bus bar 母线 oil-filled power cable 充油电力电缆 overhead line 架空线 mixed divider (阻容 混合分压器 阻容)混合分压器 阻容 transmission line 传输线 XLPE cable 交链聚乙烯电缆 (coaxial) cable (同轴 电缆 relay 继电器 同轴)电缆 同轴 iron core 铁芯 tuned circuit 调谐电路 winding 绕组 suspension insulator 悬式绝缘子 bushing 套管 porcelain insulator 陶瓷绝缘子 波头(尾 电阻 front(tail) resistance 波头 尾)电阻 glass insulator 玻璃绝缘子 inverter station 换流站 flash counter 雷电计数器 steel-reinforced aluminum conductor 充电(阻尼 阻尼)电阻 钢芯铝绞线 charging(damping) resistor 充电 阻尼 电阻 tank 箱体 point plane gap 针板间隙 earth(ground) wire 接地线 exciting winding 激磁绕组 grading ring 均压环 trigger electrode 触发电极 highvoltage engineering 高电压工程 glow discharge 辉光放电 highvoltage testing technology 高电压试验技术 harmonic 谐波 Power electronics 电力电子 Automatic control 自动控制 Principles of electric circuits 电路原理 Digital signal processing 数字信号处理

痰热清注射液联合莫西沙星治疗慢性阻塞性肺疾病急性加重期的效果

痰热清注射液联合莫西沙星治疗慢性阻塞性肺疾病急性加重期的效果
WANGJuan1,GUOQiu-ye1,LIYan-hong2
(1.Departmentofrespiratorymedicine,HanzhongCentralHospital,HanzhongShaanxi723000;2.CenterforHealthMan
agement,HanzhongShaanxi723000)
【Abstract】 Objective ToinvestigatetheclinicaleffectofTanreqingInjectioncombinedwithmoxifloxacinona cuteexacerbationofchronicobstructivepulmonarydisease(AECOPD).Methods 86patientswithAECOPD admitted from March2015toJune2017wererandomlydividedintothecontrolgroupandthetreatmentgroup,with43casesineach group.Thecontrolgroupwastreatedwithmoxifloxacinhydrochloridesodiumchlorideinjection,andthetreatmentgroupwas treatedwithTanreqingInjectiononthebasisofthecontrolgroupfor2weeks.Theclinicalefficacy,lungfunction,bloodgas analysis,inflammatoryfactorsandadversereactionsofthetwogroupswereobservedbeforeandaftertreatment.Results Aftertreatment,thetotaleffectiverate(93.02%)inthetreatmentgroupwassignificantlyhigherthanthatinthecontrol group(74.42%),andthedifferencewasstatisticallysignificant(P<0.05).Comparedwiththecontrolgroup,theFVC, FEV1,FEV1/FVCandPEFinthelungfunctionofthetreatmentgroupwereallincreased,andthePaO2,PaCO2 andpH valuesofthebloodgasanalysisindexweresignificantlyimproved.ThenumberofWBC,CRP,PCTdecreasedsignificantly, andthedifferencewasstatisticallysignificant(P0.05).Althoughthenumberofneutrophilsintheserumofthetreatment groupdecreased,thedifferencewasnotstatisticallysignificant(P>0.05).Therewasnostatisticallysignificantdifference inadversereactionsbetweenthetwogroups(P>0.05).Conclusions TanreqingInjectioncombinedwithmoxifloxacin caneffectivelyimprovethelungfunctionofpatientswithAECOPD,reducetheinflammatoryresponse,improvetheclinical treatmenteffect,andissafeandfeasible.

支气管肺炎患者给予盐酸氨溴索静脉滴入联合口服阿奇霉素的治疗效果

支气管肺炎患者给予盐酸氨溴索静脉滴入联合口服阿奇霉素的治疗效果

DOI:10.16662/ki.1674-0742.2024.07.096支气管肺炎患者给予盐酸氨溴索静脉滴入联合口服阿奇霉素的治疗效果陈阳江福建省泉州台商投资区医院儿科,福建泉州362123[摘要]目的分析口服阿奇霉素+静脉滴注盐酸氨溴索对支气管肺炎的治疗效果。

方法方便选取2020年7月—2023年7月福建省泉州台商投资区医院儿科收治的150例支气管肺炎的患儿为研究对象,以随机数表法分为对照组与研究组,每组75例。

对照组选择口服阿奇霉素治疗,研究组选择静脉滴注盐酸氨溴索+口服阿奇霉素治疗,对比两组治疗前后的症状消失时间、不良反应发生率以及炎性因子水平和动脉血气变化。

结果研究组咳嗽、发热、肺部啰音、呼吸困难等症状的消失时间分别为(3.03±0.85)、(2.82±0.65)、(2.12±0.56)、(2.05±0.44)d,短于对照组的(5.41±1.16)、(5.23±1.02)、(4.63±1.35)、(4.16±1.12)d,差异有统计学意义(t=14.332、17.256、14.873、15.185,P均<0.001)。

研究组不良反应发生率(9.33%),与对照组(6.67%)比较,差异无统计学意义(χ2=0.362,P=0.547)。

治疗前,两组血氧饱和度、肿瘤坏死因子-α、pH值、白介素-6、二氧化碳分压、C-反应蛋白、氧分压的比较,差异无统计学意义(P均>0.05)。

治疗后,研究组肿瘤坏死因子-α、白介素-6、C-反应蛋白、二氧化碳分压均低于对照组,而另外3项动脉血气指标均高于对照组,差异有统计学意义(P均<0.05)。

结论口服阿奇霉素+静脉滴注盐酸氨溴索治疗支气管肺炎,不仅可以改善患儿临床症状和动脉血气状况,还能减轻其炎症反应,安全性高。

[关键词]支气管肺炎;盐酸氨溴索;静脉滴入;阿奇霉素;治疗效果[中图分类号]R974 [文献标识码]A [文章编号]1674-0742(2024)03(a)-0096-04Therapeutic Effect of Ambroxol Hydrochloride Intravenous Infusion Com⁃bined with Oral Azithromycin in Patients with Bronchial PneumoniaCHEN YangjiangDepartment of Pediatrics, Quanzhou Taiwan Investment Area Hospital, Quanzhou, Fujian Province, 362123 China[Abstract] Objective To analyze the therapeutic effect of oral azithromycin and intravenous infusion of ambroxol hy⁃drochloride on bronchial pneumonia. Methods A total of 150 children treated with bronchopneumonia in the pediat⁃rics department of Taiwan Investment Area Hospital in Quanzhou, Fujian Province from July 2020 to July 2023 were conveniently selected as the study objects, and they were divided into control group and study group by random num⁃ber method, with 75 cases in each group. The control group was given oral azithromycin, and the study group was given intravenous infusion of ambroxol hydrochloride + oral azithromycin. The duration of symptom resolution, inci⁃dence of adverse reactions, levels of inflammatory factors and changes in arterial blood gas before and after treatment were compared between the two groups. Results The duration of cough, fever, lung rales, dyspnea and other symptoms were (3.03±0.85), (2.82±0.65), (2.12±0.56), (2.05±0.44) d, respectively. which shorter than that of control group (5.41±1.16) d, (5.23±1.02), (4.63±1.35), (4.16±1.12) d, and the differences were statistically significant (t=14.332, 17.256, 14.873, 15.185, all P<0.001). There was no significant difference in the incidence of adverse reactions between the study group (9.33%) and the control group (6.67%) (χ2=0.362, P=0.547). Before treatment, there was no significant dif⁃ference in blood oxygen saturation, tumor necrosis factor-α, pH value, interleukin-6, partial pressure of carbon diox⁃[作者简介] 陈阳江(1979-),男,本科,副主任医师,研究方向呼吸系统。

基于瘦素介导的PI3K

基于瘦素介导的PI3K

基于瘦素介导的PI3K/AKT通路探讨二甲双胍对脑卒中相关性肺炎大鼠肺损伤的作用机制李彩艳,王东枝,张冰,苏学勇,王东姝摘要目的:探究二甲双胍对脑卒中相关性肺炎大鼠肺损伤的作用及其对瘦素介导的磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)通路的影响㊂方法:无特定病原体(SPF)级雄性SD大鼠85只,随机选取12只作为假手术组,其余73只进行模型制备,其中1只造模失败,剩余72只随机分为模型组㊁瘦素组㊁瘦素+PI3K/AKT抑制剂组㊁二甲双胍组㊁二甲双胍+瘦素组㊁二甲双胍+PI3K/AKT激活剂组,每组12只㊂测定大鼠动脉血氧分压(PaO2),计算氧合指数(OI);测定各组大鼠血清瘦素㊁支气管肺泡灌洗液肿瘤坏死因子-α(TNF-α)㊁白细胞介素-1β(IL-1β)㊁C反应蛋白(CRP)水平;计算大鼠右肺湿质量/干质量;观察大鼠左肺组织病理;测定肺组织PI3K/AKT通路蛋白水平㊂结果:与假手术组比较,模型组大鼠肺部损伤加重,PaO2㊁OI水平降低(P<0.05),血清瘦素㊁TNF-α㊁IL-1β㊁CRP水平,右肺湿质量/干质量,大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT升高(P<0.05)㊂与模型组比较,瘦素组大鼠肺部损伤加重, PaO2㊁OI水平降低(P<0.05),血清瘦素㊁TNF-α㊁IL-1β㊁CRP水平,右肺湿质量/干质量,大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT升高(P<0.05);二甲双胍组大鼠肺部损伤减轻,PaO2㊁OI水平升高(P<0.05),血清瘦素㊁TNF-α㊁IL-1β㊁CRP水平,右肺湿质量/干质量,大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT降低(P<0.05)㊂与瘦素组比较,瘦素+PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠肺部损伤减轻,PaO2㊁OI水平升高(P<0.05),血清瘦素㊁TNF-α㊁IL-1β㊁CRP水平,右肺湿质量/干质量,大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT降低(P<0.05)㊂与二甲双胍组比较,二甲双胍+PI3K/AKT激活剂组大鼠肺部损伤加重,PaO2㊁OI水平降低(P<0.05),血清瘦素㊁TNF-α㊁IL-1β㊁CRP水平,右肺湿质量/干质量,大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT升高(P<0.05)㊂结论:二甲双胍对脑卒中相关性肺炎大鼠肺损伤有保护作用,可能是通过抑制瘦素介导的PI3K/AKT通路实现的㊂关键词脑卒中相关性肺炎;肺损伤;瘦素;二甲双胍;磷脂酰肌醇3-激酶/蛋白激酶B通路d o i:10.12102/j.i s s n.1672-1349.2024.09.011Effect of Metformin on Lung Injury in Rats with Stroke-related Pneumonia Based on Leptin-mediated PI3K/AKT PathwayLI Caiyan,WANG Dongzhi,ZHANG Bing,SU Xueyong,WANG DongshuSecond People's Hospital of Hengshui City,Hengshui053000,Hebei,China,E-mail:**************Abstract Objective:To explore the effect of metformin on lung injury in rats with stroke-related pneumonia and its effect on leptin-mediated phosphatidylinositol3-kinase(PI3K)/protein kinase B(AKT)pathway.Methods:A total of85male SD rats without specific pathogen(SPF)were randomly divided into sham operation group,model group,leptin group,leptin+PI3K/AKT inhibitor group, metformin group,metformin+leptin group,metformin+PI3K/AKT activator group,with12rats in each group,and1rat failed to be modeled.Arterial partial oxygen pressure(PaO2)was measured and oxygenation index(OI)was calculated.The levels of serum leptin, tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and C-reactive protein(CRP)in bronchoalveolar lavage fluid were determined in each group.The wet/dry mass of the right lung was calculated.The left lung tissue pathology was observed.PI3K/AKT pathway protein levels were determined in lung tissue.Results:Compared with sham operation group,the lung injury of model group aggravated,the levels of PaO2and OI decreased(P<0.05),the levels of serum leptin,TNF-α,IL-1β,and CRP,the wet/dry mass of right lung,the p-PI3K/ PI3K and p-AKT/AKT of lung tissue increased(P<0.05).Compared with model group,the lung injury of rats in leptin group were aggravated,the levels of PaO2and OI decreased(P<0.05),the levels of serum leptin,TNF-α,IL-1β,and CRP,the wet mass/dry mass of right lung,the p-PI3K/PI3K and p-AKT/AKT in lung tissue of rats increased(P<0.05).Compared with leptin group,the lung injury of rats in leptin+PI3K/AKT inhibitor group and metformin+leptin group reduced,the levels of PaO2and OI increased(P<0.05),the levels of serum leptin,TNF-α,IL-1β,and CRP,the wet/dry mass of right lung decreased,p-PI3K/PI3K and p-AKT/AKT decreased in lung tissue of rats(P<0.05).Compared with metformin group,metformin+PI3K/AKT activator group increased lung injury,PaO2and OI levels decreased(P<0.05),serum leptin,TNF-α,IL-1βand CRP levels,wet/dry mass of right lung,p-PI3K/PI3K and p-AKT/AKT increased in lung tissue of rats(P<0.05).Conclusion:Metformin has a protective effect on lung injury in rats with stroke-related pneumonia,which may be achieved by inhibiting leptin-mediated PI3K/AKT pathway.Keywords stroke-related pneumonia;lung injury;leptin;metformin;phosphatidylinositol3-kinase/protein kinase B pathway基金项目衡水市科技计划项目(No.2019014065Z)作者单位衡水市第二人民医院(河北衡水053000),E-mail:**************引用信息李彩艳,王东枝,张冰,等.基于瘦素介导的PI3K/AKT通路探讨二甲双胍对脑卒中相关性肺炎大鼠肺损伤的作用机制[J].中西医结合心脑血管病杂志,2024,22(9):1604-1609.脑卒中相关性肺炎的发生是脑卒中病人预后不良的重要因素,增加脑卒中的治疗难度,加重病人及家庭的经济负担,且病人极难通过治疗受益㊂因此,探寻治疗有效药物对保护病人肺功能㊁神经功能成为研究热点[1]㊂瘦素是由脂肪组织分泌的激素,可参与内分泌调节㊁创伤修复㊁免疫调节[2-3]㊂刘志敏等[4]研究显示,慢性阻塞性肺疾病(COPD)急性加重期病人血清瘦素水平与病人肺功能㊁营养状况密切相关;李俊等[5]研究显示,瘦素在肥胖成年人哮喘发病中发挥作用;瘦素可激活磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)通路在儿童变应性鼻炎中发挥免疫调节作用[6],且PI3K/AKT 通路在肺炎的发病机制中至关重要[7]㊂二甲双胍是治疗2型糖尿病的常用药物,对脑卒中具有一定的保护作用[8],且二甲双胍可治疗2型糖尿病并发肺炎,可有效降低血清炎性因子水平,减轻氧化应激反应,缩短肺炎持续时间,降低重症转化率[9]㊂此外,二甲双胍对矽肺大鼠肺炎与肺纤维化均有干预作用[10],可降低重症新型冠状病毒肺炎病死率[11]㊂本研究将基于瘦素介导的PI3K/AKT通路展开二甲双胍对脑卒中相关性肺炎肺损伤作用的研究㊂1材料与方法1.1实验动物与主要试剂无特定病原体(SPF)级雄性SD大鼠85只,体质量200~260g,购于吉林大学,许可号:SYXK(吉) 2021-0003)㊂外源性重组瘦素购自美国sigma公司; LY294002(S1105)㊁740Y-P(S7865)购自selleck公司;血清瘦素㊁肿瘤坏死因子-α(TNF-α)㊁白细胞介素-1β(IL-1β)㊁C反应蛋白(CRP)酶联免疫吸附法(ELISA)检测试剂盒购自上海酶联生物;苏木精-伊红(HE)染色试剂盒购自上海碧云天公司;磷酸化的PI3K (p-PI3K)㊁PI3K㊁磷酸化的AKT(p-AKT)㊁AKT㊁甘油醛-3-磷酸脱氢酶(GAPDH)抗体㊁羊抗兔二抗均购自abcam 公司㊂血气分析仪(Premier3500)购自上海玉研科学仪器有限公司㊂1.2方法1.2.1大鼠造模及分组取73只SD大鼠进行脑卒中相关性肺炎模型制备㊂首先使用戊巴比妥钠麻醉大鼠,仰卧位固定,颈中线开1cm切口,分离颈总动脉,用棉线制备1cm颈总动脉线环,将切口缝合,将大鼠移至立体定位仪,俯卧位沿枕骨下背中造1cm切口,在大鼠第1颈椎横突翼小孔插入注射器针头,损伤椎动脉(至鲜血溢出),止血,缝合切口,术后注射青霉素防感染㊂24h后在颈部缺口处再次打开,夹闭双侧颈动脉,15min后打开恢复血流㊂另选取12只大鼠仅暴露颈椎与总颈动脉,作为假手术组㊂造模成功标志为造模48h后大鼠进食减少,眼球浑浊,呼吸不畅,可见肺杂音[12]㊂造模成功大鼠72只,造模成功率为98.63%(72/73)㊂将成功造模大鼠随机分为模型组㊁瘦素组㊁瘦素+PI3K/AKT 抑制剂组㊁二甲双胍组㊁二甲双胍+瘦素组㊁二甲双胍+ PI3K/AKT激活剂组㊂瘦素组大鼠给予50μg/kg外源性重组瘦素腹腔注射[13];瘦素+PI3K/AKT抑制剂组大鼠除给予50μg/kg外源性重组瘦素腹腔注射外,尾静脉注射0.3mg/kg的LY294002[14];二甲双胍组大鼠给予400mg/kg二甲双胍灌胃[10];二甲双胍+瘦素组大鼠给予400mg/kg二甲双胍灌胃,50μg/kg外源性重组瘦素腹腔注射;二甲双胍+PI3K/AKT激活剂组大鼠给予400mg/kg二甲双胍灌胃,50mg/kg740Y-P 尾静脉注射[15];模型组与假手术组给予等量生理盐水灌胃㊂1.2.2大鼠动脉血氧分压(PaO2)测定采集大鼠右侧股动脉血2mL,血气分析仪分析大PaO2,计算氧合指数(OI)㊂1.2.3ELISA法检测大鼠血清瘦素水平采集大鼠股静脉血1mL,离心后获得上清液,通过ELISA试剂盒检测大鼠血清瘦素水平㊂1.2.4ELISA法测定支气管肺泡灌洗液炎性因子水平末次给药后,对所有大鼠左肺行支气管肺泡灌洗,共洗涤5次,收集肺泡灌洗液,3000r/min离心15 min,获得上清液,通过试剂盒检测TNF-α㊁IL-1β㊁CRP 水平㊂1.2.5大鼠肺组织湿质量/干质量处死大鼠,取右肺下叶滤纸擦拭至表面干燥,称重,视为湿质量;烘干后再次称质量,视为干质量,计算大鼠右肺湿质量/干质量比值㊂1.2.6HE染色观测大鼠肺组织病理改变取大鼠左肺,分为两部分,一部分常规制备肺部石蜡切片,通过HE试剂盒进行染色,封片后显微镜下观察各组大鼠肺组织病理变化;另一部分进行蛋白免疫印迹(Western Blot)实验㊂1.2.7Western Blot法测定肺组织PI3K/AKT通路蛋白水平取大鼠部分肺部组织,匀浆,12000r/min离心15 min,取上清液,经十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)电泳,将一定量蛋白转移至聚偏二氟乙烯(PVDF)膜上,封闭,加一抗p-PI3K(1:1000)㊁PI3K(1ʒ1000)㊁p-AKT(1ʒ1000)㊁AKT(1ʒ1000)㊁GAPDH(内参,1ʒ5000),孵育过夜,加入二抗(1ʒ5000),电化学发光试剂(ECL)显色液显色,分析p-PI3K㊁PI3K㊁p-AKT㊁AKT蛋白表达㊂1.3统计学处理采用SPSS22.0软件进行数据分析㊂符合正态分布的定量资料以均数ʃ标准差(xʃs)表示,多组间比较进行单因素方差分析,进一步两组间比较行SNK-q 检验㊂以P<0.05为差异有统计学意义㊂2结果2.1大鼠一般情况观察假手术组大鼠皮毛水滑,精神状态较好,饮水㊁饮食正常,体质量增长正常,有活力;模型组大鼠皮毛干枯灰色,眼睛浑浊,进食减少,饮水增多,口鼻眼分泌物增多,呼吸频率高,出现肺啰音;瘦素组大鼠较模型组症状更为明显;瘦素+PI3K/AKT抑制剂组较瘦素组症状缓解;二甲双胍组较模型组症状改善;二甲双胍+瘦素组较瘦素组症状改善;二甲双胍+PI3K/AKT激活剂组较二甲双胍组症状改善显著㊂2.2各组大鼠PaO2㊁OI比较与假手术组比较,模型组大鼠PaO2㊁OI水平降低(P<0.05);与模型组比较,瘦素组大鼠PaO2㊁OI水平降低,二甲双胍组大鼠PaO2㊁OI水平升高(P<0.05);与瘦素组比较,瘦素+PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠PaO2㊁OI水平升高(P<0.05);与二甲双胍组比较,二甲双胍+PI3K/AKT激活剂组大鼠PaO2㊁OI 水平降低(P<0.05)㊂详见表1㊂表1各组大鼠PaO2㊁OI水平比较(xʃs)单位:mmHg 组别只数PaO2OI假手术组1292.16ʃ11.51438.71ʃ54.83模型组1255.16ʃ6.50①288.65ʃ36.04①瘦素组1244.36ʃ5.54②212.17ʃ26.55②瘦素+PI3K/AKT抑制剂组1254.22ʃ5.67③265.24ʃ29.13③二甲双胍组1268.71ʃ8.58②342.56ʃ40.36②二甲双胍+瘦素组1261.55ʃ7.69③285.79ʃ35.72③二甲双胍+PI3K/AKT激活剂组1255.38ʃ6.91④276.75ʃ34.55④注:模型组与假手术组比较,①P<0.05;与模型组比较,②P<0.05;与瘦素组比较,③P<0.05;与二甲双胍组比较,④P<0.05㊂2.3各组大鼠血清瘦素比较与假手术组比较,模型组大鼠血清瘦素升高(P< 0.05);与模型组比较,瘦素组大鼠血清瘦素升高(P< 0.05),二甲双胍组大鼠血清瘦素降低(P<0.05);与瘦素组比较,瘦素+PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠血清瘦素降低(P<0.05);与二甲双胍组比较,二甲双胍+PI3K/AKT激活剂组大鼠血清瘦素升高(P<0.05)㊂详见表2㊂表2各组大鼠血清瘦素比较(xʃs)单位:ng/mL组别只数瘦素假手术组12 1.52ʃ0.19模型组12 5.72ʃ0.71①瘦素组1213.91ʃ1.13②瘦素+PI3K/AKT抑制剂组129.72ʃ1.01③二甲双胍组12 3.24ʃ0.51②二甲双胍+瘦素组12 5.28ʃ0.66③二甲双胍+PI3K/AKT激活剂组12 5.06ʃ0.61④注:模型组与假手术组比较,①P<0.05;与模型组比较,②P<0.05;与瘦素组比较,③P<0.05;与二甲双胍组比较,④P<0.05㊂2.4各组大鼠血清TNF-α㊁IL-1β㊁CRP水平比较与假手术组比较,模型组大鼠血清TNF-α㊁IL-1β㊁CRP水平升高(P<0.05);与模型组比较,瘦素组大鼠血清TNF-α㊁IL-1β㊁CRP水平升高(P<0.05),二甲双胍组大鼠血清TNF-α㊁IL-1β㊁CRP水平降低(P<0.05);与瘦素组比较,瘦素+PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠血清TNF-α㊁IL-1β㊁CRP降低(P<0.05);与二甲双胍组比较,二甲双胍+PI3K/AKT激活剂组大鼠血清TNF-α㊁IL-1β㊁CRP升高(P<0.05)㊂详见表3㊂2.5各组大鼠右肺湿质量/干质量比较与假手术组比较,模型组大鼠右肺湿质量/干质量升高(P<0.05);与模型组比较,瘦素组大鼠右肺湿质量/干质量升高(P<0.05),二甲双胍组大鼠右肺湿质量/干质量降低(P<0.05);与瘦素组比较,瘦素+ PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠右肺湿质量/干质量降低(P<0.05);与二甲双胍组比较,二甲双胍+PI3K/AKT激活剂组大鼠右肺湿质量/干质量升高(P<0.05)㊂详见表4㊂表3各组大鼠血清TNF-α㊁IL-1β㊁CRP水平比较(xʃs)组别只数TNF-α(pg/mL)IL-1β(pg/mL)CRP(mg/L)假手术组1250.11ʃ6.2626.13ʃ3.2512.16ʃ1.52模型组12147.95ʃ18.47①52.51ʃ6.56①64.18ʃ8.05①瘦素组12181.51ʃ22.68②86.79ʃ10.82②82.76ʃ10.33②瘦素+PI3K/AKT抑制剂组12155.23ʃ19.40③75.24ʃ9.62③71.64ʃ8.94③二甲双胍组12104.39ʃ13.05②40.56ʃ5.46②52.53ʃ5.66②二甲双胍+瘦素组12123.74ʃ15.42③65.34ʃ7.37③71.04ʃ8.85③二甲双胍+PI3K/AKT激活剂组12130.72ʃ16.34④68.25ʃ8.52④74.35ʃ9.26④注:模型组与假手术组比较,①P<0.05;与模型组比较,②P<0.05;与瘦素组比较,③P<0.05;与二甲双胍组比较,④P<0.05㊂表4各组大鼠右肺湿质量/干质量(xʃs)组别只数右肺湿质量/干质量假手术组12 4.32ʃ0.54模型组12 6.78ʃ0.85①瘦素组128.12ʃ1.02②瘦素+PI3K/AKT抑制剂组127.03ʃ0.86③二甲双胍组12 5.11ʃ0.75②二甲双胍+瘦素组12 6.85ʃ0.85③二甲双胍+PI3K/AKT激活剂组12 6.72ʃ0.84④注:模型组与假手术组比较,①P<0.05;与模型组比较,②P<0.05;与瘦素组比较,③P<0.05;与二甲双胍组比较,④P<0.05㊂2.6各组大鼠肺组织病理假手术组大鼠肺部切片肺泡结构完整,排列整齐,无炎性细胞浸润;模型组大鼠肺组织切片有血管扩张,肺泡腔内有炎性细胞浸润,肺泡壁变厚;与模型组比较,瘦素组大鼠肺组织肺泡腔更为狭窄,炎性细胞浸润更明显,二甲双胍组病理减轻;与瘦素组比较,瘦素+ PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠肺部病理减轻;与二甲双胍组比较,二甲双胍+PI3K/AKT激活剂组大鼠肺部病理加重㊂详见图1㊂图1各组大鼠肺部病理改变(ˑ200)2.7各组大鼠肺组织PI3K/AKT通路相关蛋白表达与假手术组比较,模型组大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT升高(P<0.05);与模型组比较,瘦素组大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT升高(P< 0.05),二甲双胍组大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT降低(P<0.05);与瘦素组比较,瘦素+PI3K/AKT抑制剂组㊁二甲双胍+瘦素组大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT 降低(P<0.05);与二甲双胍组比较,二甲双胍+PI3K/AKT 激活剂组大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT升高(P<0.05)㊂详见图2㊁表5㊂图2各组大鼠肺组织PI3K/AKT通路蛋白表达条带图(A为假手术组;B为模型组;C为瘦素组;D为瘦素+PI3K/AKT抑制剂组;E为二甲双胍组;F为二甲双胍+瘦素组;G为二甲双胍+PI3K/AKT激活剂组)表5各组大鼠肺组织PI3K/AKT通路蛋白表达比较(xʃs)组别只数p-PI3K/PI3K p-AKT/AKT假手术组120.13ʃ0.020.05ʃ0.01模型组120.72ʃ0.09①0.39ʃ0.05①瘦素组12 1.24ʃ0.15②0.82ʃ0.10②瘦素+PI3K/AKT抑制剂组120.92ʃ0.11③0.66ʃ0.08③二甲双胍组120.43ʃ0.05②0.21ʃ0.07②二甲双胍+瘦素组120.54ʃ0.06③0.69ʃ0.08③二甲双胍+PI3K/AKT激活剂组120.56ʃ0.06④0.70ʃ0.08④注:模型组与假手术组比较,①P<0.05;与模型组比较,②P<0.05;与瘦素组比较,③P<0.05;与二甲双胍组比较,④P<0.05㊂3讨论脑卒中相关性肺炎是指未行机械通气的脑卒中病人在发病7d内出现的肺炎,此肺炎的出现与脑卒中病人机体功能障碍相关,肺炎的炎症反应会进一步加剧脑卒中后脑损伤,且会引发脓毒症等严重并发症,是造成脑卒中病人预后不良的重要原因,增加病人治疗难度,缩短病人生存期㊂因此,减轻肺损伤是治疗脑卒中相关性肺炎的重点㊂本研究构建脑卒中相关性肺炎大鼠模型,造模48h 后造模大鼠出现进食减少,眼球浑浊,呼吸不畅的现象,且可闻及肺杂音,表明大鼠出现明显肺部损伤,造模型成功;此外,HE染色证实大鼠肺组织血管扩张,肺泡腔内有炎性细胞浸润,肺泡壁变厚,PaO2㊁OI水平降低,血清TNF-α㊁IL-1β㊁CRP升高,从多方面再次验证造模成功㊂瘦素在动物组织与血清中含量成正比,由脂肪组织产生,可作用于中枢神经细胞受体调控机体新陈代谢[16]㊂瘦素除在脂肪代谢中发挥调节作用外,也是一种应急类激素,出现感染后,瘦素应激性增加,感染期产生的TNF-α㊁IL-6等会刺激脂肪组织释放瘦素[17]㊂Rebello等[18]研究显示,肥胖人群新型冠状病毒肺部感染病人的高死亡率与循环瘦素介导的免疫有关;陶梅梅等[19]研究发现,老年细菌性肺炎病人血清瘦素与肺炎的严重程度相关㊂在本研究模型大鼠血清瘦素水平升高,提示瘦素与脑卒中相关性肺炎的发生有关㊂瘦素可参与对PI3K/AKT通路的调控,而PI3K/AKT 激活在脑卒中相关性肺炎中发挥促进作用[20]㊂本研究瘦素处理模型大鼠后,发现大鼠肺部损伤㊁炎症水平进一步加重,且PI3K/AKT通路被激活,此作用可被PI3K/AKT抑制剂削弱,提示瘦素可介导PI3K/AKT通路活化,可加重脑卒中相关性肺炎的肺部损伤㊂二甲双胍是常见的高效降糖药物,常应用在神经保护㊁抗炎症方面有应用[21]㊂研究显示,二甲双胍可降低2型糖尿病并发肺炎病人的乳酸和CRP水平[22];二甲双胍可通过激活线粒体活性氧物,介导对军团菌肺炎的保护作用[23];二甲双胍可降低矽肺大鼠肺纤维化[10]㊂二甲双胍在脑卒中相关性肺炎的肺损伤中是否发挥作用仍未可知㊂在本研究中,二甲双胍可降低模型大鼠肺组织p-PI3K/PI3K㊁p-AKT/AKT水平,抑制炎症反应,减轻肺损伤,提示二甲双胍在脑卒中相关性肺炎中发挥的作用可能与其他类型肺炎的作用一致,均可减轻肺损伤,且其作用机制可能与PI3K/AKT 通路有关㊂为验证二甲双胍能否作用于PI3K/AKT通路发挥作用,本研究在二甲双胍基础上加入PI3K激活剂,发现激活剂可减轻二甲双胍加重的肺炎的肺保护作用㊂此外,与瘦素激活的肺炎组比较,二甲双胍可减轻瘦素加重的肺损伤情况,并可降低瘦素诱导的PI3K/AKT 激活㊂以上结果均提示二甲双胍对脑卒中相关性肺炎大鼠肺损伤具有干预作用,且可能是通过抑制PI3K/AKT通路实现的㊂综上所述,二甲双胍可发挥对脑卒中相关性肺炎大鼠肺损伤的保护作用,可能是通过抑制瘦素介导的PI3K/AKT通路实现的㊂但二甲双胍对脑卒中相关性肺炎大鼠肺损伤的保护作用,也可能涉及其他信号通路,尚需深入研究㊂参考文献:[1]DYLLA L,HERSON P S,POISSON S N,et al.Association betweenchronic inflammatory diseases and stroke-associatedpneumonia-an epidemiological study[J].Journal of Stroke andCerebrovascular Diseases,2021,30(4):105605.[2]CHEN S,WANG Q,HAN B,et al.Effects of leptin-modified humanplacenta-derived mesenchymal 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[10]李淑娴,庞心如,严海月,等.二甲双胍对矽肺大鼠肺炎及肺纤维化的干预作用[J].中华劳动卫生职业病杂志,2021,39(10):726-732.[11]潘永红,韩睿,何勇.二甲双胍是降低重症新型冠状病毒肺炎病死率的可能选择之一?[J].中华危重病急救医学,2020,32(9):1131-1134.[12]王涛,刘宏祥,齐姣,等.羟基红花黄素A对脑卒中相关性肺炎大鼠肺组织的保护作用及机制[J].山东医药,2018,58(37):11-15. [13]张晓,秦伟伟,李秋杰,等.瘦素预处理对机械通气肺损伤大鼠NLRC4炎症小体表达的影响[J].国际呼吸杂志,2021,41(6):416-421.[14]刘小平,朱小兵,吴论.P13K-Akt-HIF-1α信号通路在右美托咪定减轻大鼠呼吸机相关性肺损伤中的作用[J].中国医药科学,2018,8(12):17-20.[15]张欣,杜文秀,刘芳,等.氨茶碱对慢性阻塞性肺疾病大鼠肺功能的改善作用[J].中华实用诊断与治疗杂志,2021,35(9):906-911. [16]柴春艳,王甜,刘娅萍,等.支气管肺癌患者血清和癌组织中瘦素水平的表达及临床意义[J].现代检验医学杂志,2020,35(4):18-21.[17]RUBIO B,MORA C,PINTADO C,et al.The nutrient sensingpathways FoxO1/3and mTOR in the heart are coordinatelyregulated by central leptin through PPARβ/δ.Implications incardiac remodeling[J].Metabolism,2021,115:154453. [18]REBELLO C J,KIRWAN J P,GREENWAY F L.Obesity,the mostcommon comorbidity in SARS-CoV-2:is leptin the link?[J].International Journal of Obesity,2020,44:1810-1817. [19]陶梅梅,马洪明,张楠,等.老年细菌性肺炎患者血清脂联素及瘦素水平与肺炎严重程度的相关性研究[J].国际呼吸杂志,2018,38(17):1287-1290.[20]CEN G Y,LIU L Y,WANG J,et al.Weighted gene co-expressionnetwork analysis to identify potential biological processes andkey genes in COVID-19-related stroke[J].Oxidative Medicineand Cellular Longevity,2022,2022:4526022.[21]ZAMANI-GARMSIRI F,GHASEMPOUR G,ALIABADI M,et al.Combination of metformin and chlorogenic acid attenuateshepatic steatosis and inflammation in high-fat diet fed mice[J].IUBMB Life,2021,73(1):252-263.[22]杨欢,张欢欢,施瑜彬,等.二甲双胍对2型糖尿病并发肺炎患者血浆乳酸和C反应蛋白水平的影响[J].实用临床医药杂志,2018,22(13):31-34.[23]KAJIWARA C,KUSAKA Y,KIMURA S,et al.Metformin mediatesprotection against legionella pneumonia through activation ofAMPK and mitochondrial reactive oxygen species[J].Journal ofImmunology,2018,200(2):623-631.(收稿日期:2022-05-17)(本文编辑邹丽)。

布地奈德雾化联合静脉注射氨溴索治疗支气管肺炎儿童的效果分析

布地奈德雾化联合静脉注射氨溴索治疗支气管肺炎儿童的效果分析

DOI:10.16662/ki.1674-0742.2023.26.086布地奈德雾化联合静脉注射氨溴索治疗支气管肺炎儿童的效果分析孙明珠,陈少华,张光林三明市第二医院儿科,福建永安366000[摘要]目的探讨支气管肺炎患儿应用布地奈德雾化联合静脉注射氨溴索治疗的临床效果。

方法简单随机选取2020年1月—2022年12月三明市第二医院救治的支气管肺炎患儿300例,以单盲分组方式划分对照组和观察组,每组150例,其中对照组给予氨溴索静脉注射疗法,观察组在参照组基础上联合雾化吸入布地奈德混悬液,比较两组的临床治疗效果。

结果观察组临床治疗总有效率为94.67%,高于对照组,差异有统计学意义(χ2=5.672,P<0.05);观察组患儿血氧饱和度、氧分压均高于对照组,且二氧化碳分压、肺泡动脉氧分压差均低于对照组,差异有统计学意义(P<0.05);观察组咳嗽、气促、干啰音、湿啰音消失时间均短于对照组,差异有统计学意义(P<0.05);观察组C反应蛋白、白介素-6、白细胞、降钙素原均低于对照组,差异有统计学意义(P<0.05)。

结论应用布地奈德混悬液联合氨溴索静脉注射治疗支气管肺炎患儿,可以加快患儿临床症状的消失,改善患儿肺功能与炎症因子水平,有助于提升临床治疗的效果,值得推荐与应用。

[关键词]小儿支气管肺炎;氨溴索;布地奈德;血气分析;炎症因子[中图分类号]R5 [文献标识码]A [文章编号]1674-0742(2023)09(b)-0086-04Effectiveness Analysis of Budesonide Nebulization Combined with Intrave⁃nous Injection of Ambroxol in Treating Children with Bronchopneumonia SUN Mingzhu, CHEN Shaohua, ZHANG GuanglinDepartment of Pediatrics, Sanming Second Hospital, Yong'an, Fujian Province, 366000 China[Abstract] Objective To observe the clinical effect of the application of budesonide nebulization combined with intra⁃venous injection of ambroxol in the treatment of children with bronchopneumonia.Methods A total of 300 children with bronchial pneumonia treated in the Second Hospital of Sanming City from January 2020 to December 2022 were selected and divided into control group and observation group by single-blind grouping, with 150 cases in each group. The control group was given intravenous ambroxol therapy, and the observation group combined with atomized budesonide suspension on the basis of the control group to compare the clinical therapeutic effects of the two groups.Results The total effective rate of the observation group was 94.67%, higher than that of the control group, and the dif⁃ference was statistically significant (χ2=5.672, P<0.05). The blood oxygen saturation and partial pressure of oxygen in observation group were higher than those in control group, and the partial pressure of carbon dioxide and the differ⁃ence of alveolar artery oxygen were lower than those in control group, and the differences were statistically significant (P<0.05). The disappearance time of cough, shortness of breath, dry rales and wet rales in observation group was shot⁃ter than that in control group, and the difference was statistically significant (P<0.05). The C-reactive protein, interleu⁃kin-6, leukocyte and procalcitonin in observation group were lower than those in control group, and the differences were statistically significant (P<0.05).Conclusion The application of budesonide suspension combined with intrave⁃nous injection of ambroxol in the treatment of children with bronchopneumonia can accelerate the disappearance of clinical symptoms, improve the children's lung function and inflammatory factor levels, and help to improve the effec⁃tiveness of clinical treatment, which is worthy of recommendation and application.[作者简介] 孙明珠(1985-),女,本科,主治医师,研究方向为儿内科(肺炎,鼻炎,哮喘)。

电能表专业术语中英文对照

电能表专业术语中英文对照

电能表专业术语中英文对照有功电度表—— watt-hour meter 静止式有功电度表—— static watt-hour meter 多费率电度表—— multi-rate meter 仪表型式—— meter type 测量器件——measuring element 测试输出—— test output工作指示器—— operation indicator 贮存器—— memory非易失贮存器—— non-volatile memory显示器—— display计度器—— register 电流线路—— current circuit 电压线路—— voltage circuit 辅助线路—— auxiliary circuit 常数—— constant 室内仪表—— indoor meter 室外仪表—— outdoor meter 表底—— base 插座—— socket 表盖—— meter cover 表壳—— meter case 可触及导电部件—— accessible conductive part 保护接地端——protective earth terminal 端子座—— terminal block 端子盖—— terminal cover 间隙—— clearance爬电距离—— creepage distance基本绝缘—— basic insulation附加绝缘—— supplementary insulation 双重绝缘—— double insulation 加强绝缘—— reinforced insulationI 类防护绝缘包封仪表—— insulating encased meter of protective class III 类防护绝缘包封仪表—— insulating encased meter of protective class II 参比电流—— reference current基本电流 *(Ib)—— basic current (Ib)额定电流 *(In)—— rated current (In)最大电流 * (Imax)—— maximum current (Imax)参比电压 * (Un)—— reference voltage (Un)参比频率—— reference frequency 等级指数—— class index 百分数误差——percentage error 影响量—— influence quantity 参比条件—— reference conditions 由影响量引起的误差改变量—— variation of error due to an influence quantity 畸变因数——distortion factor 电磁骚扰—— electromagnetic disturbance 参比温度—— reference temperature 平均温度系数—— mean temperature coefficient 额定工作条件—— rated operating conditions 规定的测量范围—— specified measuring range 规定的工作范围——specified operating range 极限工作范围—— limit range of operation 贮存和运输条件——storage and transport conditions 正常工作位置—— normal working position 热稳定性——thermal stability 型式试验—— type test 电度表型号—— meter type 标准表—— reference meter 无功功率(乏)—— reactive power(var)无功电能(乏一小时)—— reactive energy(var-hour)单相电路中无功电能—— reactive energy in a single-phase circuit 三相电路中无功电能—— reactive energy in a three-phase circuit 无功电度表—— var-hour meter 静止式无功电度表—— static var-hour meter 多费率仪表—— multi-rate meter 无功功率的方向和符号—— directions and sign of reactive power 测量元件—— measuring element 输出装置—— output devices 感应式仪表—— induction meter 仪表转子—— meter rotor仪表驱动元件—— meter driving element 仪表制动元件—— meter braking element 仪表计度器(计数机构)—— register of a meter(counting mechanism) 仪表底座—— meter base 仪表插座—— meter socket 仪表基架—— meter frame 接线端座—— terminal block 接线端盖——terminal cover 基本转速—— basic speed 基本转矩—— basic torque 仪表常数—— meter constant 绝缘—— insulation 型式—— type 型式检验—— type test 型式验证程序—— type approval procedure 鉴定程序—— qualification procedure 影响量或影响因数—— influence quantity or factor 垂直工作位置—— vertical working position 等级指数—— class index 测量单元—— measuring unit 数据处理单元—— data processing unit 多功能电能表——multifunction watthour meter 需要周期—— demand interval 最大需量—— maximum demand 滑差时间—— sliding window time 尖、峰、谷、平时段——( sharp 、peak、shoulder 、off —peak time consumption ) 额定最大脉冲频率—— rated maximum impulse frequency 最大需量复零装置—— maximum demand reset zero unit 辅助电源—— auxiliary supply 电磁骚扰—— electromagnetic disturbance 产品—— item 修理的产品—— repaired item 不修理的产品—— non-repaired item 服务—— service 规定功能—— required function 时刻—— instant of time时间区间—— time interval 持续时间—— time duration 累积时间—— accumulated time 量度—— measure 工作—— operation 修改—— modification(of an item) 效能—— effectiveness 固有能力—— capability 耐久性—— durability 可靠性—— reliability 维修性—— maintainability 维修保障性—— maintenance support performance 可用性—— availability 可信性——dependability 失效—— failure 致命失效—— critical failure 非致命失效—— non-critical failure 误用失效—— misuse failure 误操作失效—— mishandling failure 弱质失效——weakness failure 设计失效—— design failure 制造失效—— manufacturing failure 老化失效;耗损失效—— ageing failure ; wearout failure 突然失效—— sudden failure 渐变失效;漂移失效—— gradual failure ; drift failure 灾变失效—— cataleptic failure 关联失效——relevant failure 非关联失效—— non-relevant failure 独立失效—— primary failure 从属失效—— secondary failure 失效原因—— failure cause 失效机理—— failure mechanism 系统性失效;重复性失效—— systematic failure ;reproducible failure完全失效—— complete failure 退化失效—— degradation failure 部分失效—— partial failure 故障—— fault致命故障—— critical fault 非致命故障—— non-critical fault 重要故障—— major fault 次要故障—— minor fault 误用故障—— minor fault 误操作故障—— mishandling fault 弱质故障——weakness fault 设计故障—— design fault 制造故障—— manufacturing fault 老化故障;耗损故障—— ageing fault ; wearout fault 程序-敏感故障—— programme-sensitive fault 数据-敏感故障—— data-sensitive fault 完全故障;功能阻碍故障—— complete fault ;function-preventing fault 部分故障—— partial fault 持久故障—— persistent fault 间歇故障—— intermittent fault 确定性故障—— determinate fault 非确定性故障—— indeterminate fault 潜在故障—— latent fault 系统性故障—— systematic fault 故障模式—— fault mode 故障产品—— faulty item 差错—— error 失误—— mistake工作状态—— operating state 不工作状态—— non-operating state 待命状态—— standby state 闲置状态;空闲状态—— idle state ; free state 不能工作状态—— disable state ;outage 处因不能工作状态—— external disabled state 不可用状态;内因不能工作状态——down state ; internal disabled state 可用状态—— up state 忙碌状态—— busy state 致使状态—— critical state 维修—— maintenance 维修准则—— maintenance philosophy 维修方针—— maintenance policy 维修作业线—— maintenance echelon ; line of maintenance 维修约定级—— indenture level(for maintenance) 维修等级—— level of maintenance 预防性维修—— preventive maintenance 修复性维修—— corrective maintenance 受控维修—— controlled maintenance 计划性维修—— scheduled maintenance 非计划性维修—— unscheduled maintenance 现场维修—— on-site maintenance ; in sits maintenance ;field maintenance 非现场维修—— off-site maintenance 遥控维修—— remote maintenance 自动维修—— automatic maintenance 逾期维修—— deferred maintenance 基本的维修作业——elementary maintenance activity 维修工作—— maintenance action ; maintenance task 修理—— repair 故障识别—— fault recognition 故障定位—— fault localization 故障诊断——fault diagnosis 故障修复—— fault correction 功能核查—— function check-out 恢复——restoration ; recovery 监测—— supervision ; monitoring 维修的实体—— maintenance entity 影响功能的维修—— function-affecting maintenance 妨碍功能的维修—— function-preventing maintenance 减弱功能的维修—— function-degreding maintenance 不影响功能的维修—— function-permitting maintenance 维修时间—— maintenance time 维修人时——MMH maintenance man-hours 实际维修时间—— active maintenance time 预防性维修时间—— preventive maintenance time 修复性维修时间—— corrective maintenance time 实际的预防性维修时间—— active preventive maintenance time实际的修复性维修时间—— active corrective maintenance time 未检出故障时间——undetected fault time 管理延迟(对于修复性维修)—— administrative delay 后勤延迟——logistic delay 故障修复时间—— fault correction time 技术延迟—— technical delay 核查时间—— check- out time 故障诊断时间—— fault diagnosis time 故障定位时间—— fault localization time 修理时间—— repair time 工作时间—— operating time 不工作时间——non— operating time 需求时间—— required time 无需求时间—— non-required time 待命时间—— stand-by time 闲置时间—— idle time ;free time 不能工作时间—— disabled time 不可用时间—— down time 累积不可用时间—— accumulated down time 外因不能工作时间——external disabled time ; external loss time 可用时间—— up time 首次失效前时间—— time to first failure 失效前时间—— time to failure 失效间隔时间—— time between failures 失效间工作时间—— operating time between failures 恢复前时间—— time to restoration ;time to recovery使用寿命—— useful life 早期失效期—— early failure period 恒定失效密度期—— constant failure intensity period 恒定失效率期—— constant failure rate period 耗损失效期—— wear - out failure period 瞬时可用度—— A(t) instantaneous availability 瞬时不可用度—— U(t) instantaneous unavailability 平均可用度—— A(t1,t2)mean availability 平均不可用度——U(t1 , t2)mean unavailability 渐近可用度—— A asymptotic availability稳态可用度—— steady - state availability 渐近下可用度—— U asymptotic unavailability 稳态不可用度—— steady-state unavailability 渐近平均可用度—— A asymptotic mean availability 渐近平均不可用度—— U asymptotic mean unavailability 平均可用时间—— MUT mean up time 平均累积不可用时间—— MADT mean accumulated down time 可靠度——R(t1 ,t2)reliability瞬时失效率——λ (t) instantaneous failure rate平均失效率——λ (t1,t2)mean failure rate 瞬时失效密度—— Z(t) instantaneous failure intensity 平均失效密度—— Z(tl , t2) mean failure intensity 平均首次失效前时间——MTTFF mean time to first failure 平均失效前时间—— MTTF mean time to failure 平均失效间隔时间—— MTBF mean time between failures 平均失效间工作时间—— MTBF mean operating time between failures 失效率加速系数—— failure rate acceleration factor 失效密度加速系数—— failure intensity acceleration factor 维修度—— maintainability瞬时修复率——μ (t)instantaneous repair rate 平均修复率——μ (t1 , t2)mean repair rate 平均维修人时—— mean maintenance man-hours 平均不可用时间—— MDT mean down time 平均修理时间—— MRT mean repair time P—分位修理时间—— p— fractile repair time 平均实际修复性维修时间—— mean active corrective maintenance time 平均恢复前时间—— MTTR mean time to restoration 故障识别比—— fault coverage 修复比—— repair coverage 平均管理延迟—— MAD mean administrative delay p—分位管理延迟—— p-fractile administrative delay 平均后勤延迟—— MLD mean logistic delay P—分位后勤延迟—— P— fractile logistic delay 试验—— test 验证试验—— compliance test 测定试验—— determination test实验室试验—— laboratory test 现场试验—— field test 耐久性试验—— endurance test 加速试验—— accelerated test 步进应力试验—— step stress test 筛选试验—— screening test 时间加速系数—— time acceleration factor 维修性检验—— maintainability verfication 维修性验证—— maintainability demonstration 观测数据—— observed data 试验数据—— test data 现场数据—— field data 基准数据—— reference data 冗余—— redundancy 工作冗余——active redundancy 备用冗余—— standby redundancy 失效安全—— fail safe 故障裕度——fault tolerance 故障掩盖—— fault masking 预计—— prediction 可靠性模型—— reliability model 可靠性预计—— reliability prediction 可靠性分配—— reliability allocation ;reliability apportionment故障模式与影响分析—— FMEA fault modes and effects analysis 故障模式、影响与危害度分析—— FMECA fault modes , effects and criticality analysis 故障树分析—— FTA fault tree analysis 应力分析—— stress analysis 可靠性框图—— reliability block diagram 故障树——fault tree状态转移图—— state-transition diagram 应力模式—— stress madel 故障分析—— fault analysis 失效分析—— failure analysis 维修性模型—— maintainability model 维修性预计——maintainability prediction 维修树—— maintenance tree维修性分配—— maintainability allocation 老练—— burn in可靠性增长—— reliability growth可靠性改进—— reliability improvement可靠性和维修性管理——reliability and maintainability management可靠性和维修性保证——reliability and maintainability assurance可靠性和维修性控制——reliability and maintainability control可靠性和维修性大纲——reliability and maintainability programme可靠性和维修性计划——reliability and maintainability plan可靠性和维修性审计——reliability and maintainability audit可靠性和维修性监察——reliability and maintainability surveillance设计评审—— design review 真实的⋯——true ⋯预计的⋯——predicted ⋯外推的⋯——extrapolated ⋯估计的⋯——estimated ⋯固有的⋯——intrinsic ⋯;inherent ⋯使用的⋯——operationa l⋯平均的⋯——mean⋯P-分位⋯——P-fratile瞬时的⋯——instantaneous ⋯稳态的⋯—— steady state;maintainability apportionment。

探讨经纤维支气管镜灌洗联合吸入性乙酰半胱氨酸溶液对重症肺炎患者血清炎症因子的影响

探讨经纤维支气管镜灌洗联合吸入性乙酰半胱氨酸溶液对重症肺炎患者血清炎症因子的影响

DOI:10.19368/ki.2096-1782.2023.16.064探讨经纤维支气管镜灌洗联合吸入性乙酰半胱氨酸溶液对重症肺炎患者血清炎症因子的影响韩韬,孙尊鹏南京市江宁医院重症医学科,江苏南京211100[摘要]目的探究经纤维支气管镜灌洗联合吸入性乙酰半胱氨酸溶液对重症肺炎患者血清炎症因子的影响。

方法从2019年6月—2023年6月南京市江宁医院收治的重症肺炎患者中随机选择69例作为研究对象,按照随机数表法分为对照组34例、治疗组35例,分别接受经纤维支气管镜灌洗治疗、经纤维支气管镜灌洗联合吸入性乙酰半胱氨酸溶液治疗,观察不同治疗方式对重症肺炎患者血清炎症因子、血气指标的影响。

结果两组患者干预前血清炎症因子水平对比,差异无统计学意义(P>0.05);干预7 d后,治疗组C反应蛋白(C-reactive protein, CRP)水平(25.14±6.47)mg/L、肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)水平(50.24±6.31)pg/mL、降钙素原(procalcitonin, PCT)水平(0.63±0.24)ng/L均低于对照组,差异有统计学意义(t=2.716,3.160,2.730,P<0.05);干预前,两组患者血气指标对比,差异无统计学意义(P>0.05);干预7 d后,治疗组氧分压(partial pressure of oxygen,PaO2)、血氧饱和度(oxygen saturation,SaO2)高于对照组,差异有统计学意义(P< 0.05);研究组二氧化碳分压(PaCO2)低于对照组,差异有统计学意义(P<0.05)。

结论重症肺炎患者治疗中,经纤维支气管镜灌洗联合吸入性乙酰半胱氨酸溶液可改善患者血清炎症因子及血气指标,临床应用价值显著。

[关键词]重症肺炎;纤维支气管镜;灌洗;乙酰半胱氨酸溶液;血清炎症因子;血气指标[中图分类号]R4 [文献标识码]A [文章编号]2096-1782(2023)08(b)-0064-04Exploring the Effect of Trans-fiberoptic Bronchoscopic Lavage Combined with Inhaled Acetylcysteine Solution on Serum Inflammatory Factors in Patients with Severe PneumoniaHAN Tao, SUN ZunpengDepartment of Critical Care Medicine, Nanjing Jiangning Hospital, Nanjing, Jiangsu Province, 211100 China[Abstract] Objective To investigate the effect of trans-fiberoptic bronchoscopic lavage combined with inhaled acetyl⁃cysteine solution on serum inflammatory factors in patients with severe pneumonia. Methods A total of 69 patients with severe pneumonia admitted to Nanjing Jiangning Hospital from June 2019 to June 2023 were randomly selected as the study subjects, and were divided into a control group 34 patients and a treatment group 35 patients according to the random number table method, and received trans-fiberoptic bronchoscopic lavage treatment and trans-fiberoptic bronchoscopic lavage combined with inhaled acetylcysteine solution treatment, respectively. Observed the effects of different treatment modalities on serum inflammatory factors and blood gas indexes in patients with severe pneumonia.Results The serum inflammatory factor levels of the two groups of patients before intervention were compared, and the difference was not statistically significant (P>0.05). After 7 d of intervention, the levels of C-reactive protein (CRP) (25.14±6.47) mg/L, tumor necrosis factor-α (TNF-α) (50.24±6.31) pg/ml, and procalcitonin (PCT) (0.63±0.24) ng/L in the treatment group were lower than those in the control group, and the difference was statistically significant (t=2.716, 3.160, 2.730, P<0.05). Before intervention, the blood gas indexes of the two groups were compared, and the difference[作者简介] 韩韬(1987-),男,硕士,主治医师,研究方向为重症医学。

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