Essential Hypertension

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Essential hypertension

SeminarEssential hypertensionFranz H Messerli, Bryan Williams, Eberhard RitzEssential hypertension can be deﬁ ned as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac, and re nal e ve nts. In industrialise d countrie s, the risk of be coming hype rte nsive (blood pre ssure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by deﬁ nition) and this decline is the best determinant of cardiovascular risk reduction. However, diﬀ erences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular e ve nts. Most hype rte nsive patie nts ne e d two or more drugs for blood-pre ssure control and concomitant statintreatment for risk factor reduction. Despite the availability of eﬀ ective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients. Introduction“The treatment of the hypertension itself is a diﬃ cultand almost hopeless task in the present state of our knowledge and in fact, for ought we know the hypertension may be an important compensatory mechanism which should not be tampered with even if it were certain that we could control it.”1With these words in 1931, Paul Dudley White described what is nowadays regarded as a common misconception about the clinical signiﬁ cance of essential hypertension: namely, that the increase in blood pressure was essential (or compensatory) to guarantee adequate perfusion of the target organs. Regrettably, this misconception lingered in published work (and in many doctors’ minds) until a few years ago, despite the results of the Veterans’ Administration studies 2,3attesting to the beneﬁ ts of antihypertensive treatment. Since then, ﬁ ndings of many trials have shown unequivocally that lowering blood pressure reduces cardiovascular morbidity and mortality for hypertension of all degrees of severity and even in high-risk normotensive individuals. As of July 1, 2007, a Medline search with the term “essential hypertension” retrieved a total of 22 376 articles, of which 3430 were reviews. Rather than attempting to review this work, we will focus here on a few key and emerging issues that we think are of interest to clinicians dealing with hypertensive cardiovascular disease. Ambulatory versus casual blood-pressure measurementsDiagnosis and treatment of hypertension hinges on correct measurement of blood pressure (panel 1). However, this seemingly simple procedure poses manypitfalls and—apart from the introduction of 24-h ambulatory blood-pressure measurement and automated self measurement—has progressed littlebeyond the procedure that Korotkoﬀintroduced 100 years ago.4As Kaplan noted: “The measurement of [blood pressure] is likely the clinical procedure of greatest importance that is performed in the sloppiest manner.”5 Diagnosis of hypertension should be based ideally onseveral blood-pressure measurements taken on separate days, as stated in guidelines.6 For this purpose, the mercury sphygmomanometer has an unsurpassed accuracy,7 but it has been substituted by aneroid and auscultatory or oscillometric semiautomatic devices. Aneroid manometers must be serviced and recali-brated periodically. The reliability of wrist blood-pressure measurements with oscillatory devices is limited.8,9 Home blood-pressure measurement permits identi ﬁ cation of so-called white-coat hypertension (see next section) correlates better than blood-pressurevalues measured in the doctor’s oﬃ ce with target-organdamage,10and could enhance patients’ adherence todrugs.White-coat hypertension and masked hypertensionBecause the correlation between 24-h ambulatory blood-pressure measurements and those taken in the doctor’s oﬃ ce is moderate, the diagnosis of hypertension can be missed by oﬃ ce blood-pressure measurements in some patients who are truly hypertensive (masked hypertension). Conversely, blood pressure can be raisedSearch strategy and selection criteria We scanned the leading journals that publish basic and clinical research in the area of hypertensive cardiovascular disease and searched Medline. The main terms we used were: “essential hypertension”, “cardiovascular disease”, “lifestyle modiﬁ cation”, and “antihypertensive drug therapy”. Additionally, the thoughts and input of our collaborators and colleagues and the reviewers of this Seminar were also considered.Lancet 2007; 370: 591–603 See Editorial page 539St Luke’s-Roosevelt Hospital Center, New York, NY, USA (F H Messerli FACP); Universityof Leicester School of Medicine,Leicester, UK(Prof B Williams MD); and University of Heidelberg, Heidelberg, Germany(Prof E Ritz MD)Correspondence to:Dr Franz H Messerli, Division of Cardiology, St Luke’s-RooseveltHospital Center, ColumbiaUniversity, College of Physiciansand Surgeons, 1000 TenthAvenue, New York, NY 10019,USAfmesserli@Seminarin the doctor’s oﬃce but not on ambulatory blood-pressure monitoring or at home—a situation known as white-coat hypertension. Risk of patients having white-coat hypertension was noted to be somewhat higher than in normotensive individuals but distinctly lower than in people with sustained hypertension.11–15 By contrast, masked hypertension is a less well known (but not necessarily a less frequent) entity with a more serious prognosis than white-coat hypertension. It was noted in as many as a third of the hypertensive population.16,17 In participants of the PAMELA study,18 those with masked hypertension had a higher prevalence of echocardiographic left-ventricular hypertrophy than did normotensive individuals. Inappropriate target-organ disease (for oﬃ ce blood-pressure levels) should trigger suspicion of masked hypertension and motivate doctors to undertake 24-h ambulatory blood-pressure monitoring in a patient. Upper limits for optimum, normal, and hypertensive blood-pressure levels have been redeﬁ ned (table).19 Importantly, rises in blood pressure in the doctor’s oﬃ ce, at home, and while ambulatory seem to have an additive eﬀ ect on cardiovascular risk.20Compared with white-coat hypertension, masked hypertension needs to be looked for and there are few clinical hints to its presence. Because most patients take their medication for hypertension in the morning, blood-pressure values in the doctor’s oﬃ ce usually are normal but can be raised at the end of the dosing interval (ie, during early morning hours). Many patients are still prescribed once-a-day atenolol—a drug that does not reduce heart attack or strokes. Atenolol’s ineﬃ ciency might be related to inappropriate duration of action, its pseudo-antihypertensive eﬀect, or both (see next section). For many clinicians, masked hypertension has unfortunately become a blind spot in antihypertensive treatment.21With respect to the therapeutic approach, we should remember that white-coat hypertension can only be over-treated; therefore, a conservative approach to treatment is justiﬁ ed. Conversely, masked hypertension has a more serious prognosis than white-coat hypertension and can only be under-treated; it deserves, therefore, an aggressive diagnostic and therapeutic approach.Aortic versus brachial blood pressureSince the pulse wave is ampliﬁ ed in transit from the heart to the brachial artery, central aortic systolic pressure is usually lower than brachial pressure.22 The magnitude of ampliﬁ cation is greatest in people with healthy compliant arteries and diminishes with age. Systolic pressure within the aorta is a composite of two items: 1) the outgoing pressure wave, generated by ventricular contraction; and 2) pressure wave reﬂ ection from periphery. The reﬂ ected wave should ideally return towards the heart during diastole to augment diastolic ﬁ lling. If it returns earlier during the cardiac cycle it ampliﬁ es the outgoing pressure wave and leads to an increase in central aortic pressure. The timing and magnitude of pressure-wave reﬂection is aﬀ ected by several factors, including: the stiﬀ ness of the aorta; the distance of reﬂection sites from the heart; and heart rate.As a result, brachial pressure can be an imperfect surrogate for central aortic pressure, particularly when drug treatments diﬀ erentially aﬀ ect central aortic haemodynamics, wave reﬂection, heart rate, or a combination.23 Findings of the CAFE study, in which pulse-wave analysis was used to derive central aortic pressures, showed that β blocker-based treatment was signiﬁcantly less eﬀective than a calcium-channel blocker-based regimen at lowering aortic systolic pressure and pulse pressure, despite identical brachialPanel 1: Points to consider for blood-pressure measurement in the doctor’s oﬃ ce• The patient should sit for several minutes in a quiet room before blood-pressure measurements are taken. Pain,stress, full urinary bladder, a recent meal, and talking oractive listening during measurement aﬀ ect bloodpressure• Take at least two measurements spaced by 1–2 min and additional measurements if the ﬁ rst two are quitediﬀ erent• Using a bladder that is too narrow yields false high readings. Instead of the standard bladder (12–13 cm long,35 cm wide) use an appropriate bladder in patients withincreased midarm circumference• Use phase I (ﬁ rst tapping sound) and V (disappearance) Korotkoﬀ sounds to identify systolic and diastolicblood-pressure values, respectively• Do not deﬂ ate the cuﬀ too rapidly, otherwise individual Korotkoﬀ sounds are missed and too low a value ismeasured; start with a deﬂ ation rate of 2 mm/s• Measure the heart rate by palpation and watch out for arrhythmia, which mandates repeated blood-pressuremeasurements• At the ﬁ rst visit, measure blood pressure in both arms and take the higher value as the reference; measure bloodpressure at 1 and 5 min after standing upright if thepatient has a disorder that frequently causes orthostatic hypotensionSeminar pressures in both treatment arms.24pseudo-antihypertensive eﬀ ect could account for whyβ blocker-based strategies are less eﬀ ective thanalternative treatments at regressing end-organ damageand in prevention of stroke.24–27 Whether central aorticpressure is a better predictor of outcome thanconventional brachial blood pressure remains to beestablished.Hypertension as a gateway to cardiovascularrisk managementAlthough measurement of blood pressure is a simpleprocedure to identify a risk phenotype of cardiovasculardisease, treatment of raised blood pressure alone isinsuﬃcardiovascular disease risk, and formal cardiovasculardisease risk estimation has been recommended. Riskcalculations based on the Framingham cohort used inthe USA and the UK28,29 can overestimate risk in Europeanpopulations by about 7% and by a larger proportion inrecommended use of the SCORE risk calculator.30Pragmatism in risk assessment is important, andavailable risk calculators are based on conventional riskmarkers that can be recorded in a basic clinicalsetting—ie, systolic blood pressure, age, sex, cholesterolconcentration, presence of diabetes, smoking history,and presence or absence of structural damage. Findingsof the INTERH EART study suggested that more than90% of population-attributable risk for acute myocardialinfarction can be accounted for by these risk factors.31Use of more elaborate risk assessment by a series ofbiomarkers adds little to the aforementioned conventionalmethods of cardiovascular disease risk estimation.32One of the most relevant criticisms of cardiovasculardisease risk estimation is that it is based on limited time projections—eg, 10-year absolute risk estimations—that strongly favour treatment of the elderly population versus young people because age is a powerful determinant of short-term risk. Additional factors contributing to and amplifying risk are diabetes30,33 and renal malfunction, as indicated by a low estimated glomerular ﬁ ltration rate34,35 and microalbuminuria or proteinuria.36 For both microalbuminuria and proteinuria, the conventional cutoﬀ points are arbitrary, particularly for albuminuria.37 Equally random is that a serum creatinine concentration of 107–133 µmol/L is a sign of target-organ damage and an amount greater than 133 µmol/L indicates renal disease. Assessment of renal malfunction was enhanced by estimation of the glomerular ﬁltration rate, taking into account age, sex, and body-mass index.38 Cardiac abnormalities by electrocardiography39 or echocardiography40 are correlated to outcome. Figure 1 outlines progression of the natural history of hypertensive cardiovascular disease. In a study of the natural history of (untreated) hypertension in control groups, wide variability of the absolute risk of stroke and heart attack was noted (ﬁ gure 2), but the relation between number ofevents prevented and absolute risk was near-linear forboth coronary heart disease and stroke.41Cardiovascular disease risk thresholds for interventioncurrently deﬁne high-risk patients as having a 10-yearFramingham-derived cardiovascular disease risk of 20% ormore. The typical hypertensive man aged 55 years or olderwill have this level of risk. This threshold takes account ofcurrent evidence and economics, and lower thresholds forintervention would also be cost eﬀective with existingcriteria for cost-beneﬁ t analyses.32 Of note, formalcardiovascular disease risk estimation is not necessary forpatients with hypertension and cardiovascular disease,diabetes, or overt end-organ damage. These patients are atsuﬃcient risk of cardiovascular disease to beneﬁ t frommultifactorial risk-factor intervention.The prothrombotic paradoxHypertension by deﬁ nition is a haemodynamic disorderand, as such, exposes the arterial tree to increasedpulsatile stress. Paradoxically, however, most majorcomplications of longstanding hypertension (ie, heartPrehypertensionProteinuriaNephrosclerosisEstablished hypertensionChronicrenalfailureCoronaryVentricularFigure 1: Range of hypertensive cardiovascular disease from prehypertension to target-organ damage and end-stage diseaseSeminarattack and strokes) are thrombotic rather than haemorrhagic, referred to as the so-called thrombotic paradox of hypertension. Virchow suggested three components facilitating thrombus formation: 1) damage to the vessel wall; 2) hypercoagulability; and 3) abnormal blood ﬂ ow. For thromboembolic events to take place, all the components of Virchow’s triad must be fulﬁ lled.42 In hypertensive individuals, abnormalities in blood ﬂ ow have been well recognised. Hypertension has also been associated with endothelial damage or dysfunction43 and a hypercoagulable state.42 This prothrombotic state could be the result of chronic low-grade inﬂ ammation. Chronic shear stress can lead to remodelling of the vascular endothelium, turning it from an anticoagulant into a procoagulant surface.The mechanisms leading to endothelial dysfunction are multifactorial and include decreased activity of vasodilator agents44–46 and increased activity (or sensitivity) to vasoconstrictor agents.45–47 Overall, ﬁ brinolytic activity is ascertained by the balance between tissue plasminogen activator and plasminogen activator inhibitor type 1 (SERPINE1). With respect to endothelial function, enhanced activity of the renin-angiotensin system and kallikrein-kinin system has opposite eﬀ ects, resulting in vasoc onstriction and vasodilation, respectively.48 By con t rast, with respect to coagulation, increased activity of the renin-angiotensin system and the kallikrein-kinin sys t em has a negative eﬀ ect, resulting in a hypercoagulable state.48 Thus, hypertension not only confers a hyper c oag u lable state(vulnerable blood) but also gives rise to left-ventricular hypertrophy, ventricular and atrial arrhyth m ias, and impaired coronary reserves (vulnerable myo c ar d ium),thereby fulﬁ lling all criteria for a vulnerable patient.49In enhancing the coagulation-ﬁ brinolysis balance, anti-hypertensive treatment can decrease the frequency of throm b o tic events independent of blood pressure. Whetherdiﬀ erences in antihypertensive drug classes48,50,51 will trans-late into altered outcomes remains to be established. Prehypertension and lifestyle interventionsThe issue of prehypertension has stirred tempers to an extent that seems more suitable to medieval theologians than modern scientists.52 Epidemiological evidence suggests a continuous relation between risk of cardiovascular disease and usual blood-pressure values of at least 115/75 mm Hg.53 In the Framingham cohort,a stepwise increase in cardiovascular events was reported in individuals with high baseline blood pressure within the normotensive range.54 Thus, in people without hypertension (blood pressure <140/90 mm H g), blood-pressure levels parallel cardiovascular disease risk in the same way as hypertension.55 Therefore, normotensive individuals with a host of risk factors could show higher overall risk than mildly hypertensive patients without risk factors. Furthermore, the absolute beneﬁ ts of antihypertensive treatment for such normotensive people can be greater than for uncomplicated hypertensive patients.Since individuals without hypertension still outnumber those with the disorder, the blood-pressure-related disease burden remains larger in the normotensive than the hypertensive population.55 Irrespective of the level of hypertension, lowering of blood pressure is always preferable by non-pharmacological means, such as a low salt diet, weight loss, exercise, and alcohol restriction. Indeed, a small but signiﬁ cant fall in blood pressure was noted in meta-analyses of these interventions (ﬁ gure 3).56–59 However, patients’ adherence to lifestyle interventions is notoriously poor; therefore, antihypertensive treatment might have to be considered even in some normotensive individuals. Since the beneﬁts in this population are fairly small, such an approach needs documents of long-term safety. Thus, drugs with metabolic side-eﬀ ects, such as β blockers and diuretics, are not suitable to be used in prehypertensive patients. Also, angiotensin-converting-enzyme inhibitors should probably be avoidedFigure 2: Correlation between absolute risk of coronary heart disease or stroke event in selected clinical trials and number of events prevented per 1000 patient-years of treatmentRelation between absolute risk and event prevented is steeper for stroke than for coronary heart disease, possibly because stroke is more dependent on blood pressure. Unweighted correlation coeﬃ cients were: r=0·89, p<0·0001 for stroke (dashed line), and r=0·87, p<0·0001 for coronary heart disease (solid line). Only trials in which 100 or more events were reported are included. Symbols are drawn encompassing an area proportional to the number of events in every trial. DIABHYCAR=DIABetes and HYpertension Cardiovascular events with Ramipril. DutchTIA=Dutch Transient Ischemic Attack trial. EUROPA=EUropean Reduction Of cardiac events with Perindopril in stable coronary Artery disease. EWPHE=European Working Party on Hypertension in the Elderly. FEVER=Felodipine EVEnts Reduction trial. HDFP=Hypertension Detection and Follow-up Program. HOPE=Heart Outcomes Prevention Evaluation. IDNT=Irbesartan Diabetes Nephropathy Trial. MRC=Medical Research Council Trial (in mild hypertension). MRC-E=Medical Research Council Trial in Older Patients.PATS=Post-stroke Antihypertensive Treatment Study. PEACE=Prevention of Events with Angiotensin-Converting Enzyme inhibition. PROGRESS=Perindopril pROtection aGainst REcurrent Stroke Study. QUIET=QUinapril Ischemic Events Trial. RENAAL=Reduction of Endpoints in Non-Insulin Dependent Diabetes Mellitus with the Angiotensin II Antagonist Losartan trial. SCOPE=Study on COgnition and Prognosis in the Elderly. SHEP=Systolic Hypertension in the Elderly Program. Syst-China=Systolic hypertension in China trial. Syst-EUR=Systolic hypertension in Europe trial.41Seminarbecause of risk for angio-oedema. The only two drug classes that presently fulﬁ l safety requirements are angiotensin-receptor blockers and some calcium-channel blockers. Indeed, in two studies (TROPH Y and PH ARAO), treatment of prehypertensive patients with renin-angiotensin system blockers delayed the onset of stage I hypertension and prolonged the hypertension-free period.60,61We certainly are not advocating treatment of all prehypertensive patients, which could be up to 45 million in the USA alone. However, in those with high-normal blood pressure and diabetes, or a history of cerebrovascular or coronary disease, evidence suggests that antihypertensive drugs are beneﬁ cial. Clearly, the timehas come to abandon the hypertension/normotension dichotomy and to focus on global risk reduction, either by antihypertensive drugs, lipid-lowering treatment, or their combination. New-onset diabetes with antihypertensivetreatmentEver since the report of Colin Dollery’s team more than 20 years ago,62,63 diuretic treatment—particularly when combined with a β blocker—has been known to increase risk for new-onset diabetes. From 1980 to 2004, the prevalence of diabetes more than doubled in the USA,and almost 10% of people older than age 20 years have this disease.64 Patients with hypertension are known to be at higher risk of developing new-onset diabetes than normotensive individuals. In the ALLH AT study, about 10% of all patients developed the disorder throughout the duration of the study.65However, the relative risk was 18% and 40% higher in the chlorthalidone arm than in the amlodipine and lisinopril arms, respectively.66In a network meta-analysis, Elliott and Meyer reported the odds ratio of new-onset diabetes to be 0·62 with angiotensin-receptor blockers, 0·67 with angiotensin-converting-enzyme inhibitors, 0·75 with placebo, 0·79 with calcium-channel blockers, and 0·9 with β blockers; diuretics were the reference.67Admittedly, risk for new-onset diabetes associated with β blockers, diuretics, or both 68 seems to be small. Over a 4-year period, in ALLH AT , the absolute risk was 3·5% higher with chlorthalidone than with lisinopril,65 and in ASCOT , risk was 2·5% higher in the atenolol arm than in the amlodipine arm.69 However, since in the USA alone about 20 million patients are on thiazide diuretics and an almost equal number are on β blockers, this risk translates into 250 000 cases of new-onset diabetes associated withthese so-called traditional antihypertensive drugs everyyear. This ﬁgure would indicate that about 20–25% of the 1 million cases of new-onset diabetes arising yearly in the USA could possibly be related to antihypertensivetreatment—not an insigniﬁcant number. An anonymous statement was published in the BMJ in 2003: “It can’t get clearer. Diuretics—the leastexpensive and most eﬀective agents—should be the ﬁ rst line treatment for almost everyone with hypertension,including patients with diabetes.”70 We beg to diﬀ er and think that in uncomplicated hypertension, diuretics and β blockers should no longer be considered for ﬁ rst-line treatment. The trade-oﬀ of lowering blood pressure at the expense of increasing risk for diabetes by up to 10% yearly is not acceptable. Not unexpectedly, Thomas Sydenham’s dictum of primum non nocere also appliesto ﬁrst-line antihypertensive treatment. First-line antihypertensive treatment and concomitant risk factor reductionThe most important question to ask when selecting initial drug treatment is which class of drug will deliver the most eﬀ ective blood-pressure lowering for thispatient? This question is most relevant becauseblood-pressure lowering is the driver of beneﬁt and initial reductions seem to be a determinant of early cardiovascular disease risk reduction and long-term quality of blood-pressure control.71,72 The response to diﬀ erent classes of drugs is similar when compared head-to-head in heterogeneous populations. H owever, individual responses can diﬀ er strikingly. Somecharacteristics can help predict the initial response to drugs that lower blood pressure. Blood-pressure lowering in older patients (eg, those older than age55 years) or those of black ethnic origin at any age will generally be greatest with thiazide-type diuretics orcalcium-channel blockers.65,71,72 In young people, who generally have a more active renin-angiotensin system than older individuals, blood pressure is loweredeﬀ ectively with inhibitors of the renin-angiotensinsystem—eg, angiotensin-converting-enzyme inhibitors or angiotensin-receptor blockers.73,74 Such stratiﬁ cationfor selection of drug type has been adopted by some guidelines, emphasising that eﬃ ciency of blood-pressure control should drive initial drug selection.75 For patients whose blood pressure is already 20 mm H g or more above their goal, guidelines recommend initial treatmentwith a two-drug combination because monotherapy is likely to be insuﬃ cient.76,77 If ﬁ ndings of an ongoing study 78conﬁ rm safety and eﬃ cacy then initial treatmentFigure 3: Estimated decrease in blood pressure mediated bynon-pharmacological intervention in hypertension56–59Seminarwith a combination of two drugs is likely to become common practice.High-risk patients with hypertension should not only undergo optimum blood-pressure control (with two drugs) but also receive a statin and low-dose aspirin.29,30 This strategy would halve deaths from cardiovascular disease in high-risk patients at a cost of less than US$1000 per quality-adjusted life-year gained.32 Traditional thinking about cardiovascular disease risk factors as individual entities has, unfortunately, impeded this idea of combined risk factor intervention.The complicated and refractory hypertensive patientRefractory (or resistant) hypertension is deﬁ ned as blood pressure that is persistently higher than target—ie, 140/90 mm H g for most hypertensive patients and 130/80 mm H g for individuals with diabetes or renal disease—despite prescription of three diﬀ erent antihypertensive drug classes, including a diuretic. Refractory hypertension is seen freq u ent-ly. Even in most controlled trials the mean achieved blood pressure failed to reach targets.79 Poor blood-pressure control in primary care,80 particularly in elderly people,81 is not surprising but, nevertheless, disquiet-ing because of the high associated cardiovascular risk.82,83 Two categories of refractory hypertension can be distinguished: 1) true resistance; and 2) apparent resistance .84True resistancePanel 2 summarises factors that can lead to true resistant hypertension. Most patients in this category can be treated by omitting relevant drugs and altering the antihypertensive drug regimen. In a few individuals, secondary causes of hypertension can be noted.One major step forward in management of patients with true resistance has been recognition that inappropriate aldosterone concentrations (raised aldosterone/renin ratio) arise in up to 20% of people,85–87 including hypertensive emergencies.88Although patients are frequently normokalaemic,89 only a few have surgically correctable adenoma.90Irrespective of whether or not an adenoma is present, aldosterone antagonists provide relevant additional blood-pressure reduction 85,87,91,92independent of aldosterone concen t rations. H yper-kalaemia is rare,85 at least as long as renal function is not impaired.Apparent resistanceA typical cause of faulty blood-pressure measurement is use of a cuﬀ that is too small relative to the circumference of the arm, particularly in obese individuals. The blood-pressure value taken in the doctor’s oﬃ ce mightalso be raised if the patient smoked or had coﬀ ee before their appointment. A less frequent occurrence is malfunction of the measuring device used by the patient. A rare cause is so-called pseudohypertension as a result ofstiﬀor calciﬁ ed brachial arteries, which should be suspected if either measured blood-pressure values are inappropriate for target-organ damage or antihypertensivedrugs provoke symptoms of hypotension despite persistent raised blood pressure. Non-speciﬁc but helpful is Osler’s manoeuvre—ie, a palpable radial artery when the brachial artery is occluded.93 Another common cause of apparent refractoryhypertension is an inadequate drug regimen—ie,insuﬃcient dosing, selection of inadequate combi-nations of drugs, and choice of antihypertensive agentswith insuﬃcient duration of action. The solution is long-acting well-tolerated drugs or drug combinations, including a diuretic, taken once a day.94 Arguably the most frequent cause of apparent resistant hypertensionis non-adherence to treatment.Non-adherence to treatment“I’ve also been treating the high cholesterol and then Istopped the medicine because I got my cholesterol down low. And, I had in the past, a little [blood pressure]problem, which I treated and then I got it down…” (Former US President Clinton, awaiting coronary bypass surgery, calls into Larry King Live from his hospital bed; posted Friday, Sept 3, 2004, 23:31 h EST).Panel 2: True resistant hypertensionVolume overload• Excessive dietary sodium intake• Compensatory response to vasodilatory antihypertensive drugs • Insuﬃ cient diuretic treatment • Reduced renal function • HyperaldosteronismContraindicated drugs or exogenous substances • Non-steroidal anti-inﬂ ammatory drugs, COX2 inhibitors • Sympathicomimetics (nasal drops, appetite suppressants)• Cocaine • Oral contraceptives • Glucocorticoids • Mineralocorticoids • Liquorice • Herbal drugs (ginseng, yohimbin)• Drugs (eg, erythropoietin, cyclosporin, tacrolimus)• Diﬀ erent types of drugs can also aﬀ ect pharmacokinetics and cause rapid inactivation of antihypertensive drugs Associated condition • Smoking • Obesity (visceral obesity)• Metabolic syndrome or type 2 diabetes • Excess alcohol intake• Anxiety-induced hyperventilation or panic attacks • Pain。

高血压病

29
常用降压药物---①利尿剂（Diuretic）
– 噻嗪类、袢利尿剂、保钾利尿剂 – 降压机制：排钠，减少血容量，降低外周血管阻力 – 副作用: 低钾，影响血糖、血脂、血尿酸 – 保钾利尿剂可引起高血钾
30
常用降压药物---①利尿剂（Diuretic）
类别噻嗪类适应征心衰，老年高血压，单纯收缩期高血压肾功能不全，心衰痛风禁忌征强制性可能妊娠
11.88 7.73 5.11
1959
1979
1991
2002年
8
流行病学
• 我国高血压的“三低”：知晓率低、治疗率低、控制率低知晓率（%）治疗率（%）控制率（%)
中国
1991年 2002年
26.3 30.2 60 70
12.1 24.7 40 59
2.8 6.1 25 34
美国
1980年 2000年
90~99 100~109 ≥110 ＜90
注：以上为成人高血压标准，儿童则采用不同年龄组血压值 6 的95%位数。
血压水平与心血管发病危险之间的关系是连续的。血压从115/75mmHg开始，每升高20/10mmHg，心血管危险增加1倍!
7
流行病学
近50年来，我国高血压患病率快速上升
高血压患病率（ % ） 20 18 16 14 12 10 8 6 4 2 0 18.8
10
高血压的发病机制
1. 交感神经系统活性亢进
病因感N CNS功能异常儿茶酚胺神经递质，交阻力血管收缩
2. 肾性水钠潴留
交感N亢进/肾血管阻力增加、肾小球微小的结构病变、肾内/外排钠激素、潴钠激素。
11

减重手术治疗原发性高血压

减重手术治疗原发性高血压陆佳军(综述);朱江帆(审校)【摘要】[Summary] Obesity is the most important risk factor of essential hypertension.Obesity-related hypertention has become a worldwide problem.Many clinical studies show that bariatric surgery has significant therapeutic effect on essential hypertension, but the specific mechanism of the condition remains to be fully understood.This paper tried to explainthe mechanism of the treatment of bariatric surgery for essential hypertension from the following two aspects: the reversal of the sympathetic disorder and the decline of plasma leptin.%肥胖是原发性高血压第一危险因素，肥胖性高血压已成为一个不容忽视的全球性问题。

许多临床研究证实，减重手术对原发性高血压有明显的治疗效果，但机制尚未完全阐明。

本文着重从交感神经紊乱逆转和血浆瘦素的下降阐述减重手术治疗原发性高血压可能的机制。

【期刊名称】《中国微创外科杂志》【年(卷),期】2015(000)012【总页数】4页(P1125-1128)【关键词】减重手术;原发性高血压【作者】陆佳军(综述);朱江帆(审校)【作者单位】大连医科大学，大连 116044; 同济大学附属东方医院肥胖与代谢病外科，上海 200123;大连医科大学，大连 116044; 同济大学附属东方医院肥胖与代谢病外科，上海 200123【正文语种】中文【中图分类】R656.6+1;R544.1随着生活水平的提高及人们饮食习惯的改变，肥胖人群日益增多，肥胖是原发性高血压的危险因素之一。

临床实验报告英文

Title: Evaluation of the Efficacy and Safety of a New Antihypertensive Drug in Patients with Essential HypertensionIntroduction:Hypertension, also known as high blood pressure, is a common chronic condition affecting millions of people worldwide. It is a major risk factor for cardiovascular diseases, including stroke, myocardial infarction, and heart failure. The aim of this clinical trial was to evaluate the efficacy and safety of a new antihypertensive drug, Drug X, in patients with essential hypertension.Materials and Methods:Study Design:This was a randomized, double-blind, placebo-controlled, parallel-group clinical trial. The study duration was 12 weeks.Participants:A total of 200 patients with essential hypertension were enrolled in the study. The inclusion criteria were as follows:1. Age between 18 and 70 years2. Diagnosed with essential hypertension according to the American Heart Association guidelines3. Systolic blood pressure (SBP) ≥ 140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 m mHg at baseline4. Willingness to comply with the study protocolExclusion Criteria:1. Patients with secondary hypertension or other cardiovascular diseases2. Patients with a history of allergic reactions to the study drug orits active ingredients3. Patients on concurrent antihypertensive medications4. Patients with severe liver or kidney dysfunction5. Pregnant or lactating womenRandomization and Blinding:Participants were randomly assigned to two groups: the Drug X group and the placebo group. The randomization process was performed using a computer-generated randomization list. Both the participants and the investigators were blinded to the treatment allocation.Interventions:The participants in the Drug X group received Drug X at a dose of 10 mg once daily, while the participants in the placebo group received a matching placebo. All participants continued their baseline antihypertensive therapy throughout the study.Outcome Measures:The primary outcome measure was the change in SBP and DBP from baseline to the end of the study. Secondary outcome measures included the proportion of participants achieving blood pressure control (SBP < 140 mmHg and DBP < 90 mmHg), the incidence of adverse events, and the changes in laboratory parameters.Data Analysis:The data were analyzed using descriptive statistics, including means, standard deviations, frequencies, and percentages. The primary and secondary outcome measures were compared between the two groups using the independent t-test or chi-square test, as appropriate. The safety analysis was performed using descriptive statistics, and adverse events were categorized based on the World Health Organization's Common Terminology Criteria for Adverse Events (CTCAE).Results:Of the 200 enrolled participants, 191 completed the study. Baseline characteristics were similar between the two groups. At the end of the study, the mean change in SBP from baseline was -15.2 mmHg in the Drug Xgroup and -8.5 mmHg in the placebo group (p < 0.001). The mean change in DBP from baseline was -9.8 mmHg in the Drug X group and -5.2 mmHg in the placebo group (p < 0.001). The proportion of participants achieving blood pressure control was 78% in the Drug X group and 38% in the placebo group (p < 0.001).The incidence of adverse events was similar between the two groups, with the most common being dizziness, headache, and nausea. All adverse events were mild to moderate in severity and resolved without any intervention.Conclusion:The results of this clinical trial demonstrate that Drug X is an effective and safe antihypertensive agent in patients with essential hypertension. The drug significantly reduced SBP and DBP, leading to a higher proportion of participants achieving blood pressure control. The adverse event profile was favorable, with no significant differences between the Drug X group and the placebo group.Recommendations:Based on the findings of this study, Drug X can be considered as a potential treatment option for patients with essential hypertension. Further research is needed to evaluate the long-term efficacy and safety of the drug in a larger population.Authors' Contributions:- Author 1: Conceived and designed the study, collected and analyzed the data, and wrote the manuscript.- Author 2: Contributed to the study design, analyzed the data, and reviewed the manuscript.- Author 3: Provided statistical analysis and reviewed the manuscript.Conflict of Interest:The authors declare no conflicts of interest.Funding:This study was funded by [Funding Source Name].Ethical Approval:The study was approved by the Institutional Review Board [IRB Name] and was conducted in accordance with the Declaration of Helsinki.Acknowledgments:We thank the participants for their contribution to this study.References:- [List of references]。

高血压名词解释基础护理学

高血压名词解释基础护理学高血压（Hypertension）是指人体动脉血压长期持续升高的一种疾病。

可以分为原发性高血压和继发性高血压。

原发性高血压也称为essential hypertension，是指血压升高的原因不明确，可能与遗传、环境、生活方式等因素有关。

继发性高血压是指高血压是由其他疾病或药物引起的，如肾脏疾病、心脏病、甲状腺问题等。

下面是一些与高血压相关的基础护理学名词的解释：1. 血压（Blood pressure）：指心脏收缩和舒张时血液对动脉壁产生的压力。

2. 收缩压（Systolic pressure）：指心脏收缩时动脉内的最高压力。

3. 舒张压（Diastolic pressure）：指心脏舒张时动脉内的最低压力。

4. 高血压病期（Stages of hypertension）：将高血压按血压水平分为不同的阶段。

常见的分期有高血压前期、一级高血压、二级高血压和三级高血压。

5. 高血压危险因素（Risk factors for hypertension）：指可能导致高血压发生的因素，包括年龄、遗传因素、体重超标、高盐摄入、饮酒和缺乏运动等。

6. 血压控制（Blood pressure control）：指通过生活方式改变、药物治疗等手段，使患者的血压保持在正常范围内，预防并控制高血压相关并发症的发生。

7. 血压计（Sphygmomanometer）：用于测量血压的仪器，主要包括袖带、压力计和听诊器等组成部分。

8. 抗高血压药物（Antihypertensive drugs）：用于治疗高血压的药物，包括钙通道阻滞剂、ACE抑制剂、β受体阻滞剂、利尿剂等。

这些药物可以通过不同的途径降低血压。

以上是一些高血压相关的基础护理学名词的解释，希望对您有帮助。

Antihypertensive Drugs-Cardiovascular Pharmacology抗高血压,心血管药理学

Cardiac Output X Peripheral Resistance = Arterial Pressure
Since the product of heart rate and stroke volume equals cardiac output, an increase
in heart rate will increase arterial blood pressure, all other factors remaining equal.
Adrenergic Neuron Blocker
Guanethidine Reserpine
Adrenoceptor Antagonists
Labetalol (alpha & beta) Prazosin (alpha) Terazosin (alpha)
Vasodilators
Diazoxide Hydralazine Minoxidil Nitroprusside sodium
Angiotensin Converting Enzyme Inhibitors (ACEI)
Benazepril Captopril Enalapril Fosinopril Quinapril Ramipril
Angiotensin Receptor Blocker
Saralasin Losartan Irbesartin
Peripheral resistance:
For a given cardiac output, blood pressure depends only on peripheral resistance. Some antihypertensive drugs act to reduce peripheral resistance.

医学英语翻译与写作MedicalEnglishTranslationandwriting

English Translation and the Chinese Attainment
To avoid a lack of subjects
1. In regard to the operation tomorrow, it is postponed. 2. Only with large numbers of patients can we be confident that a small difference between two forms of treatment will be detected. 3. As it is digested slowly, milk sugar remains in the intestinal tract for a longer period than do other sugars.
English Translation and the Chinese Attainment
To decrease English-style expressions
Illness prevented him from going there. 原译：疾病妨碍他去那里。（此译文不符合汉语的表达习惯，主要是因为这种译法硬按原文的语法结构来翻译。此句的关键是将原文中的宾语him译成汉语中的主语“他”）改译：他因病未去那里。
Translation and English Grammar
1. The patient is not so sick but he should be hospitalized. 2. When you exercise vigorously, waste products which act as mild poisons to the nervous system are formed. 3. From this you can find out the ratio of oxygen reacting to water formed.

高血压病患者生活方式的健康教育及护理干预

高血压病患者生活方式的健康教育及护理干预AbstractHypertension is a chronic non-communicable disease characterized by high blood pressure. It is a major risk factor for cardiovascular diseases, stroke, and kidney failure. Hypertension has an incredibly high prevalence worldwide, with an increasing trend in developing countries. The lifestyle of hypertensive patients plays a critical role in the prevention and management of hypertension. Health education and nursing interventions are essential strategies that can help hypertensive patients to improve theirlifestyle and achieve better blood pressure control. This paper discusses the health education and nursinginterventions that have been used to manage hypertension in various countries worldwide.IntroductionHypertension, also known as high blood pressure, is a chronic non-communicable disease affecting millions of people worldwide. According to the World Health Organization (WHO), hypertension is defined as a systolic blood pressure of 140 mmHg or higher, and/or a diastolic blood pressure of 90 mmHg or higher. Hypertension is a significant risk factor for cardiovascular diseases, stroke, chronic kidney disease, and other complications (1).Global prevalence of hypertension is rising rapidly, and it is estimated that approximately one billion peopleworldwide have hypertension. Moreover, hypertension is responsible for about 9.4 million deaths annually worldwide, making it one of the leading causes of death globally (2, 3).Lifestyle interventions constitute the first-line management of hypertension. Appropriate lifestyle changes can lower blood pressure (BP) and reduce the need for medication.Health education and nursing interventions play an essential role in the management and prevention of hypertension. Therefore, this paper aims to review health education and nursing interventions that are effective in managing hypertension and improving the quality of life of hypertensive patients.Health EducationHealth education is the process of educating people about health and disease prevention, to help them improve their health and well-being. The goal of health education in hypertension management is to raise awareness among patients about their condition and how to control it. Health education for hypertension includes information on the cause and risk factors for hypertension, its complications, lifestyle modifications, and the significance of adherence to medication (4).Effective health education strategies for hypertension may include the following:1. Stress management trainingStress is a significant risk factor for hypertension. Therefore, teaching patients methods of managing stress such as relaxation exercises can help lower blood pressure (5).2. Dietary modificationsHealth education on dietary modifications is essential in hypertension management. Hypertensive patients need to beeducated about dietary changes such as reducing salt intake, increasing potassium intake, and avoiding excess alcohol and caffeine (6).3. Physical activityRegular physical activity is essential in hypertension management. Hypertensive patients should be encouraged to engage in moderate-intensity physical activity such as brisk walking, cycling, or swimming for at least 30 minutes every day (6).4. Smoking cessationSmoking cessation is crucial in hypertension management. Hypertensive patients who smoke should be advised to quit smoking to prevent further damage to the blood vessels (7).5. Medication adherenceHealth education on medication adherence is essential in hypertension management. Patients should be advised to adhere to prescribed medication, the correct dosages, and frequencies to achieve better blood pressure control (8).Nursing InterventionsThe role of nurses in hypertension management is significant. Nurses have a crucial role in helping hypertensive patients to achieve better blood pressurecontrol and improve their quality of life. Nursing interventions that may help in hypertension management include the following:1. Blood pressure monitoringBlood pressure monitoring is an essential component of hypertension management. Nurses can monitor and record the patient's blood pressure regularly and provide feedback to the patient on blood pressure control (9).2. Lifestyle modificationsNurses can educate hypertensive patients about lifestyle modifications such as dietary changes and physical activity. Nurses can also provide guidance in making small but sustainable changes in lifestyle (10).3. Medication managementNurses can help in medication management by reminding patients to take their medication, ensuring the correct medication, dose, and frequency. Additionally, nurses can monitor the side effects or adverse effects of medication and report them to the physician (11).4. Patient education on self-careNurses can educate hypertensive patients on self-monitoring, self-care, and importance of adherence to medication to control blood pressure. Patient education onself-care also includes adherence to follow-up appointments with physicians and regular blood pressure monitoring at home (9).5. Collaborative careCollaborative care involves collaboration among nurses, physicians, and other healthcare professionals to manage hypertension effectively. Collaborative care is crucial in hypertension management, taking into consideration the significant comorbidities that hypertensive patients may have, such as diabetes and obesity (12).ConclusionHypertension is a significant global health problem that affects millions of people worldwide. The lifestyle of hypertensive patients plays a crucial role in hypertension management. Health education and nursing interventions are essential to help hypertensive patients achieve better blood pressure control and improve their quality of life. Healtheducation strategies include stress management training, dietary modifications, physical activity, smoking cessation, and medication adherence. Nursing interventions include blood pressure monitoring, lifestyle modifications, medication management, patient education on self-care, and collaborative care. Effective hypertension management requires a collaborative approach among nurses, physicians, and other healthcare professionals.。

内科学英文课件：Hypertention

Classification of Hypertension
➢Hypertension
Essential Hypertension 原发性高血压（高血压病）90–95%
Secondary Hypertension继发性
高血压
5–10%
①primary or essential hypertension: high blood pressure with no obvious underlying(潜在的,根本的) medical crtension: High blood pressure that is caused by another medical condition(医疗条件) or medication(药物).
➢Primary or Essential Hypertension
Benign Hypertension (Chronic Hypertension) 良性/ 缓进性高血压
Hypertention
What Is Hypertension?
Definition:(1)Hypertension (HTN or HT), also known as high blood pressure or arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated.
Epidemiology
In the US: • 70% of the hypertensives are aware that
they have hypertension • 59% are being treated • Only 34% have adequately controlled BP

中医《病理学》课件-高血压病

4
2020/8/6
二、高血压病的类型
类型病发病发血压病变特
程年龄病
点
率
预后
缓进长 35-40
缓慢分三期，晚期出现内
型
10- 岁以 95% ↑ ，细A透脏功能不全，
（良 20 后，
波动明变多死于脑出
性）年
→固
血。
定
急进短青、
急剧分期不半-1年内死
型急中年 5% ↑，明，细亡，大多死
三期：视乳头水肿，蛋白渗出和出血（视
力障碍)
15
2020/8/6
高血压病 essential hypertension
四、病因与发病机理：
1、精神因素（中枢N学说）； 2、肾缺血（肾素学说） 3、肾上腺皮质作用（内分泌学说） 4、其他因素：遗传因素、年龄因素、职业与环境因素
5、摄钠过多学说。
16
③无血管、心、脑、肾的器质性病变。
6
2020/8/6
高血压病 essential hypertension
2、动脉病变期：
①全身细、小A持续性痉挛+细A硬化→血压升
高；
②血压高，较稳定。舒张压一般在110mmHg左右，难降至正常；
③有动脉硬化和早期内脏改变：
a、细A玻变；
b、小A内膜增生+平滑肌细胞增生—壁厚；
脑组织缺血坏死 → 脑软化。一般为小灶性，影
14
响不大；大者多并出血，出现相应定位症状 2020/8/6
高血压病 essential hypertension
（五）视网膜
高血压病时视网膜血管病变大致与高血压病三个时期的变化一致用眼底镜检查可见如下病变：

essential短语

essential短语
以下是一些 Essential 短语的示例：
- essential services：必要服务
- essential for：对...是必不可少的；对...是至关重要的
- essential oil：（林）精油；挥发油；香精油；植物精油
- essential amino acid：（生化）必需氨基酸；非必需氨基酸；必须氨基酸
- essential tremor：特发性震颤；家族遗传性震颤；发性震颤
- essential fatty acid：（生化）必需脂肪酸；必须脂肪酸；必需脂酸；脂肪酸- essential hypertension：原发性高血压；高血压病；高血压；特发性高血压
- essential singularity：本质奇点；（数）本性奇点；本性奇性
- essential thrombocytosis：原发性血小板增多症；特发性血小板增多症
- essential nutrient：必需营养素；必要养分；必需的营养物
- essential information：重要信息；（自）基本信息
Essential 可以与不同的词汇搭配，表达不同的意思，如果你想了解更多关于Essential 的短语，可以继续向我提问。

9脂联素

Blockade of the Renin-Angiotensin System Increases Adiponectin Concentrations in Patients WithEssential HypertensionMasato Furuhashi,Nobuyuki Ura,Katsuhiro Higashiura,Hideyuki Murakami,Marenao Tanaka,Norihito Moniwa,Daisuke Yoshida,Kazuaki ShimamotoAbstract—Adiponectin,an adipocyte-derived protein,has been suggested to play an important role in insulin sensitivity.We examined the association between insulin sensitivity(M value)evaluated by the euglycemic-hyperinsulinemic glucose clamp and adiponectin concentrations in30essential hypertensives(EHT)and20normotensives(NT)and investigated the effect of blockade of the renin-angiotensin system(RAS)on adiponectin concentrations.EHT were divided into12insulin-resistant EHT(EHT-R)and18non–insulin-resistant EHT(EHT-N)using meanϪ1SD of the M value in NT.There were no intergroup differences in age,gender,and body mass index(BMI).EHT-R had significantly higher levels of insulin and triglyceride and lower levels of adiponectin than did NT and EHT-N.EHT-R had higher levels of free fatty acid and lower levels of high-density lipoprotein(HDL)cholesterol than did EHT-N.Adiponectin concentrations were positively correlated with M value and HDL cholesterol and negatively correlated with BMI, insulin,free fatty acid,and triglyceride but not with blood pressure.M value,BMI,and HDL cholesterol were independent determinants of adiponectin concentrations in multiple and stepwise regression analyses.Sixteen EHT were treated with an angiotensin-converting enzyme inhibitor(temocapril,4mg/d;nϭ9)or an angiotensin II receptor blocker (candesartan,8mg/d;nϭ7)for2weeks.Treatment with temocapril or candesartan significantly decreased blood pressure and increased M value and adiponectin concentrations but did not affect BMI and HDL cholesterol.These results suggest that hypoadiponectinemia is related to insulin resistance in essential hypertension and that RAS blockade increases adiponectin concentrations with improvement in insulin sensitivity.(Hypertension.2003;42:76-81.) Key Words:adiponectinⅢhypertension,essentialⅢinsulin resistanceⅢrenin-angiotensin systemA dipose tissue was once thought to be simply a depot forfuel storage in the form of triglyceride.However,it is now known that adipocytes secrete a variety of proteins,such as tumor necrosis factor(TNF)-␣,plasminogen activator inhibitor-1,leptin,resistin,and adiponectin.These proteins are implicated in a wide range of biological effects.Adi-ponectin,an adipocyte-derived protein referred to as Acrp30, apM1,AdipoQ,and GBP28,has been independently identi-fied and characterized.1–5In contrast to other adipocyte-derived proteins,the circulating levels of adiponectin are reduced in patients with coronary artery disease and in states of insulin resistance such as obesity and type2diabetes.6–8 Adiponectin has been suggested to enhance insulin sensitivity and prevent atherosclerosis.9,10Furthermore,thiazolidinedio-nes,currently being used as insulin sensitizers in the treat-ment of type2diabetes,have been shown to enhance the mRNA levels and plasma levels of adiponectin in human subjects and animal models of insulin resistance and type2 diabetes.11–13Insulin resistance and accompanying hyperinsulinemia have been linked to the onset and progression of hypertension and atherosclerosis.It has been shown that approximately 40%of essential hypertensives are insulin-resistant.14,15Al-though there have been2recent studies on the concentrations of adiponectin in patients with essential hypertension,16,17the results are inconsistent.In those studies,some subjects had been taking antihypertensive drugs,which might influence insulin sensitivity,and a method for reliable and direct assessment of insulin sensitivity such as the euglycemic-hy-perinsulinemic glucose clamp method was not used.In addition,antihypertenisve drugs such as angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers have been reported to improve insulin sensitivi-ty,18,19but there are no reports on the relationship between adiponectin concentrations and blockade of the renin-angio-tensin system(RAS).We therefore examined the association between insulin sensitivity assessed by the euglycemic-hyperinsulinemic glu-cose clamp technique and adiponectin concentrations in patients with essential hypertension as well as the effect of RAS blockade on adiponectin concentrations in patients with essential hypertension.Received February26,2003;first decision March19,2003;revision accepted May14,2003.From the Second Department of Internal Medicine,Sapporo Medical University School of Medicine,Sapporo,Japan.Correspondence to Masato Furuhashi,M.D.,Ph.D.,Second Department of Internal Medicine,Sapporo Medical University School of Medicine,S-1, W-16,Chuo-ku,Sapporo060–8543,Japan.E-mail furuhasi@sapmed.ac.jp©2003American Heart Association,Inc.Hypertension is available at DOI:10.1161/01.HYP.0000078490.59735.6E76MethodsStudy Protocol1Two groups of subjects were enrolled in this study:30mild-to-moderate essential hypertensive patients(EHT,mean age: 46.4Ϯ10.6years)and20body mass index(BMI)-matched normo-tensive subjects(NT,mean age:45.6Ϯ13.9years).The subjects had been taking no medication or had stopped taking all drugs that may affect insulin sensitivity at least2weeks before the start of the study. None of the subjects had any evidence of complications such as endocrine or metabolic disturbances,cerebrovascular or cardiovas-cular disease,or renal disease.All of the subjects were hospitalized and were put on a regular diet(2000kcal/d)that included310g of carbohydrate,50g of fat,80g of protein,120mmol of sodium,and 75mmol of potassium for more than1week.Insulin sensitivity was evaluated as the M value(metabolic clearance of glucose,mg·mϪ2·minϪ1)by the euglycemic-hyperinsulinemic glucose clamp tech-nique.MeanϪ1SD of the M value in the NT was chosen as the cutoff point for insulin resistance.On the basis of this value,the EHT were divided into two groups:one group of insulin-resistant EHT (EHT-R)and one of non–insulin-resistant EHT(EHT-N).Before the clamp study,blood pressure was measured and blood samples were obtained from all of the subjects.The concentrations of adiponectin, glucose,insulin,and lipid variables were measured.This study was performed with the approval of the ethics committee of our institu-tion,and informed consent was obtained from all of the subjects. Study Protocol2We also examined the effect of RAS blockade on insulin resistanceand serum adiponectin concentrations in patients with essential hypertension.Sixteen patients with essential hypertension were recruited from the EHT in study protocol1and treated with an angiotensin-converting enzyme inhibitor,temocapril(4mg/d,nϭ9), or an angiotensin II receptor blocker,candesartan(8mg/d,nϭ7),for 2weeks in hospital.Insulin sensitivity was evaluated by glucose clamp study before and after treatment.Blood samples were obtained before the clamp study.Euglycemic-Hyperinsulinemic GlucoseClamp TechniqueA2-hour euglycemic-hyperinsulinemic glucose clamp was per-formed according to the method described by DeFronzo et al.20A vein in a forearm was cannulated for blood glucose monitoring. During the glucose clamp,blood was continuously withdrawn at2.0 mL/h through a catheter.In addition,a contralateral antecubital vein was cannulated with a plastic cannula for the infusion of insulin and glucose.Continuous insulin infusion,monitoring of glucose concen-tration,and infusion of various amounts of glucose in order to clamp glucose levels in the basal state were performed with a model STG-22artificial endocrine pancreas(Nikkiso Corp).The infusion rate of insulin(humalin R U-40,Shionogi Pharmaceutical Co)was 40mU·mϪ2·minϪ1.During insulin infusion,euglycemia was maintained by infusion of a20%glucose solution.The mean rate of glucose infusion for the last30minutes of the clamp was used as an index of insulin sensitivity(M value).The M value was expressed as milligrams of glucose per square meter of body surface area. Laboratory InvestigationsSerum adiponectin level was measured using a commercially avail-able sandwich enzyme-linked immunosorbent assay kit(Otsuka Pharmaceuticals Co,Ltd)as previously reported.5Fasting plasma glucose was determined by the glucose oxidase method.Fasting plasma insulin was measured by a radioimmunoassay method (Insulin RIA bead,Dianabot).Serum lipid profiles,including total cholesterol,high-density lipoprotein(HDL)cholesterol,triglyceride, and free fatty acid(FFA),were estimated by enzymatic methods. Statistical AnalysisNumeric variables are expressed as meanϮSD in protocol1and as median(range)in protocol2.Group statistical comparisons were assessed by one-way analysis of variance and␹2test.Linear regression analysis was used to determine the correlation between2 variables.Multiple linear regression analysis was performed by using serum adiponectin level as a dependent variable and age, gender,BMI,mean blood pressure,M value,HDL cholesterol, triglycerides,and FFA as independent variables.Stepwise regression analysis was also performed in a forward direction with F for the entry set to4,showing the percentage of variance in the adiponectin concentration that significant independent variables explained(r2). The difference between2paired variables in protocol2was analyzed by Wilcoxon signed rank test.A probability value ofϽ0.05was considered statistically significant.ResultsStudy Protocol1The EHT showed a significantly higher mean blood pressure and a lower M value than did the ing a cutoff point of meanϪ1SD of the M value in the NT,the EHT were divided into two groups:one group of12EHT-R and one group of18 EHT-N.As shown in Table1,there were no intergroup differences in age,gender,and BMI.Mean blood pressures in the EHT-R and EHT-N were comparable.The EHT-R had significantly higher levels of fasting insulin and triglyceride than did the NT and EHT-N.The EHT-R had higher levels of FFA and lower levels of HDL cholesterol than did the EHT-N.The levels of fasting plasma glucose and total cholesterol in the three groups were similar.No significant differences were found between lipid variables in the NT and EHT-N.In all of the subjects,the M value was negatively correlated with the levels of fasting insulin(rϭϪ0.57, PϽ0.01)and FFA(rϭϪ0.44,PϽ0.01).The EHT-R had significantly lower levels of serum adi-ponectin concentrations than did the NT and EHT-N(Table 1).Although adiponectin concentrations were significantly higher in women than in men(6.3Ϯ2.0versus 4.8Ϯ2.0␮g/mL,PϽ0.01),serum adiponectin concentrations in the TABLE1.Basal Characteristics and Metabolic Variables of Study SubjectsVariablesNT(nϭ20)EHT-N(nϭ18)EHT-R(nϭ12) Age,y45.6Ϯ13.946.3Ϯ9.746.3Ϯ12.1 Men/Women,n10/109/95/7 Body mass index,kg/m224.5Ϯ2.724.7Ϯ2.925.3Ϯ2.5 Mean blood pressure,mm Hg93.4Ϯ10.7111.5Ϯ13.9*106.3Ϯ21.0* M value,mg·m–2·min–1184.6Ϯ46.5197.9Ϯ41.2120.3Ϯ13.9*†Fasting plasma glucose,mmol/L 4.9Ϯ0.5 4.8Ϯ0.4 4.9Ϯ0.6 Fasting insulin,pmol/L29.2Ϯ13.923.7Ϯ8.748.5Ϯ28.7*†Total cholesterol,mmol/L 4.9Ϯ0.9 4.7Ϯ1.0 4.6Ϯ1.0 HDL cholesterol,mmol/L 1.1Ϯ0.3 1.1Ϯ0.30.9Ϯ0.1†Triglyceride,mmol/L0.9Ϯ0.40.9Ϯ0.4 1.3Ϯ1.0*†Free fatty acid,mmol/L0.51Ϯ0.260.34Ϯ0.170.62Ϯ0.39†Adiponectin,␮g/mL 5.7Ϯ2.3 6.0Ϯ2.1 4.2Ϯ1.4*†Values are expressed as number(n)or meanϮSD.NT indicates normoten-sive subjects;EHT-N,essential hypertensive patients with no insulin resistance; EHT-R,essential hypertensive patients with insulin resistance;and M value, metabolic clearance rate of glucose as an index of insulin sensitivity.Group comparisons were assessed by one-way analysis of variance and the␹2test. *PϽ0.01vs NT;†PϽ0.01vs EHT-N.Furuhashi et al Adiponectin and Renin-Angiotensin System Blockade77EHT-R were lower than those in the NT and EHT-N regardless of gender.In all of the subjects,serum adiponectin levels were positively correlated with the M value (r ϭ0.44,P Ͻ0.01)and HDL cholesterol levels (r ϭ0.51,P Ͻ0.01)and negatively with BMI (r ϭϪ0.62,P Ͻ0.01)and levels of fasting insulin (r ϭϪ0.39,P Ͻ0.01),FFA (r ϭϪ0.29,P Ͻ0.05),and triglyceride (r ϭϪ0.33,P Ͻ0.05)but not cor-related with mean blood pressure.Multiple regression anal-ysis showed that gender,the M value,BMI,and HDL cholesterol levels were independently correlated with the serum adiponectin concentrations.Stepwise regression anal-ysis also revealed that gender,the M value,BMI,and HDL cholesterol levels were independent determinants of adi-ponectin concentrations,explaining a total of 67%of the variance in this measure (r 2ϭ0.67).Study Protocol 2Treatment with temocapril or candesartan significantly de-creased mean blood pressure and FFA levels and increased the M value (Table 2).Fasting insulin levels were decreased,but not significantly,by treatment with temocapril (P ϭ0.06)or candesartan (P ϭ0.08).There were no significant changes in BMI and levels of fasting plasma glucose,total cholesterol,HDL cholesterol,and triglyceride.Both temocapril and can-desartan significantly increased adiponectin concentrations (Figure).There were mean 15%and 30%increases in adiponectin levels after treatment with temocapril and can-desartan,respectively.Adiponectin concentrations were in-creased in 15of the 16patients.The change in M value was significantly correlated with that in adiponectin concentra-tions (r ϭ0.59,P Ͻ0.05).There was no significant difference between the changes in adiponectin levels by treatment in men and women.DiscussionFour notable findings were obtained in the present study.First,adiponectin concentrations in insulin-resistant essential hypertensives were lower than those in normotensives andnon –insulin-resistant hypertensives,suggesting that hypoadi-ponectinemia in essential hypertensives is attributable to insulin resistance.This finding is in accordance with previous findings that adiponectin levels are reduced in states of insulin resistance such as obesity and type 2diabetes.7,8Second,adiponectin levels were significantly correlated with the degree of insulin sensitivity in the whole body (M value)estimated by glucose clamp study,and the M value was an independent predictor of adiponectin concentration.Third,our findings are generally consistent with previous findings in Japanese women of a positive association between adiponec-tin concentrations and HDL cholesterol levels.21This rela-tionship was independent of obesity and insulin sensitivity in the present study.Finally,RAS blocking agents such as temocapril and candesartan increased adiponectin levels with accompanying improvement in insulin sensitivity but did not affect the degree of adiposity.To the best of our knowledge,TABLE 2.Change of the Metabolic Variables by TreatmentVariables Temocapril (n ϭ9)Candesartan (n ϭ7)BeforeAfterBeforeAfterAge,y 54(34–66)51(30–78)Men/Women,n 6/33/4Body mass index,kg/m 226.4(20.5–29.6)26.0(20.6–28.9)22.5(20.5–28.5)22.9(20.6–27.8)Mean blood pressure,mm Hg 121.0(95.7–144.0)103.7(100.3–137.3)*101.5(79.1–116.7)91.8(70.2–109.8)*M value,mg ·m –2·min –1156.8(100.5–277.5)179.1(127.7–312.2)*151.9(125.9–196.2)219.9(140.8–307.8)*Fasting plasma glucose,mmol/L 4.6(4.2–5.9) 4.7(4.3–5.7) 4.7(4.2–9.6) 4.7(4.2–8.3)Fasting insulin,pmol/L 24.6(16.8–71.4)20.4(18.0–44.4)26.4(18.0–44.4)19.2(18.0–31.2)Total cholesterol,mmol/L 5.3(2.9–7.2) 5.3(3.1–8.2) 4.2(3.4–6.4) 4.5(3.5–6.6)HDL cholesterol,mmol/L 1.0(0.7–1.8) 1.2(0.6–2.0) 1.0(0.8–1.9) 1.1(0.7–1.8)Triglyceride,mmol/L 0.9(0.5–2.6)0.8(0.4–3.7) 1.0(0.6–2.3)0.7(0.5–1.5)Free fatty acid,mmol/L0.38(0.25–0.88)0.32(0.19–0.78)*0.34(0.22–0.59)0.27(0.11–0.42)*Values are expressed as number (n)or median (range).The difference between 2paired variables was analyzed by Wilcoxon signed rank test.*P Ͻ0.05vs beforetreatment.Adiponectin concentrations in patients with essential hyperten-sion before and after 2-week treatment with temocapril (4mg/d)or candesartan (8mg/d).Both temocapril and candesartan sig-niﬁcantly increased adiponectin concentrations.White and black circles represent men and women,respectively.The difference between 2paired variables was analyzed by Wilcoxon signed rank test.*P Ͻ0.05.78Hypertension July 2003this is the first report on the effect of RAS blockade on circulating adiponectin concentrations.Both temocapril and candesartan,which were used in the present study,have been reported to improve insulin sensi-tivity.18,19Several possible mechanisms of improvement in insulin sensitivity by RAS blockade have been suggested.22 Angiotensin II has been shown to increase serine phosphor-ylation of the insulin receptor,insulin receptor substrate1, and phosphatidylinositol-3-kinase(PI3K),which result in an impairment of insulin signaling.23A possible mechanism of improvement in insulin sensitivity is that RAS blockade causes inhibition of the impairment of insulin signaling by angiotensin II,resulting in activation of the glucose trans-porter and its translocation from an intracellular membrane compartment to a plasma membrane fraction.Other mecha-nisms may include the following:vasodilation,which in-creases the blood flow in skeletal muscle;24an increase in the ratio of insulin-sensitive type1fiber in muscle fiber compo-sition;25and a decrease in TNF-␣in skeletal muscle.26An increase in adiponectin levels caused by RAS blockade may also be a novel mechanism for RAS blockade–mediated enhancement of whole-body insulin sensitivity. However,the precise mechanisms by which RAS blockade leads to an increase in circulating adiponectin levels are unclear.It has been suggested that adiponectin levels can be increased after weight reduction.8,27RAS blockade,however, did not affect BMI in the present study.We speculate that the mechanisms of an increase in adiponectin concentrations may include the following processes.First,the increase in serum adiponectin levels could be the result of enhanced insulin sensitivity.It has been reported that insulin infusion during a glucose clamp study leads to a decrease in adiponectin concentrations,28suggesting that chronic hyperinsulinemia associated with an insulin-resistant state leads to a decrease in adiponectin concentrations.This raises the idea that the effect of RAS blockade on adiponectin levels is,at least partly,mediated by the decrease in insulin levels,which is secondary to the effect of RAS blockade on enhancing insulin sensitivity.Although administration of thiazolidinediones,peroxisome proliferator-activated recep-tor(PPAR)␥agonists,has been shown to increase adiponec-tin concentrations,11–13treatment with metformin,a non–PPAR␥-associated antihyperglycemic agent,or fenofibrate,a PPAR␣agonist that has recently been shown to improve insulin sensitivity,29has been reported to have no effect on adiponectin concentrations in mice.13This indicates that the change in adiponectin concentrations is not simply a conse-quence of an improved metabolic phenotype and that the change in adiponectin levels is indeed(directly or indirectly) RAS blockade–mediated.Second,based on results of recent in vitro studies showing that angiotensin II markedly inhibits adipogenic differentia-tion of human adipocytes via the angiotensin type I receptor and that expression of angiotensin II–forming enzymes in adipose tissue is inversely correlated with insulin sensitivity, Sharma et al30have hypothesized that RAS blockade pro-motes the recruitment and differentiation of preadipocytes and that increased formation of small insulin-sensitive adipo-cytes counteracts the ectopic deposition of lipids in muscle and liver,thereby improving insulin sensitivity.With regard to thiazolidinediones,it has been shown in a previous study that15-day treatment with troglitazone did not change the total weight of white adipose tissues but increased the number of small adipocytes and decreased the number of large adipocytes.31Adiponectin secretion may be directly affected by adipocyte differentiation.RAS blockade is likely to promote an increase in adipogenesis that may result in a greater net capacity for adiponectin production.However, because the hypothesis by Sharma et al has not been proved yet in vivo,further investigations of adipogenesis during a relatively short period of RAS blockade seem to be needed. Moreover,the increase in adiponectin levels caused by RAS blockade may be regulated at a level of post-transcription,including translation and/or secretion,because the magnitude of increase in adiponectin levels caused by RAS blockade for2weeks in the present study was low compared with the previously reported130%increase in circulating adiponectin concentrations in normal glucose-tolerant subjects after14-day treatment with rosiglitazone,a PPAR␥agonist.13It has also been reported that angiotensin II does not influence the gene expression of adiponectin in 3T3-L1adipocytes.32The fact that insulin-stimulated adi-ponectin exocytosis in3T3-L1adipocytes is mediated in a PI3K-dependent fashion33may be relevant to a post-translational mechanism,because angiotensin II has been shown to inhibit insulin-mediated PI3K activity.23 Lastly,since it has been shown that TNF-␣suppresses expression and secretion of adiponectin in3T3-L1adipo-cytes11and that RAS blockade decreases TNF-␣levels in skeletal muscle and mononuclear cells but not yet confirmed in adipose tissue,26,34the increase in adiponectin secretion could be caused by a decrease in TNF-␣levels or actions in adipocytes.The influence of candesartan on serum adiponectin con-centrations seems to be greater than that of temocapril in the present study.However,the mean change in the M value caused by candesartan was higher,but not significantly,than that caused by temocapril.Because change in the M value was correlated with change in adiponectin concentrations,the difference between changes in adiponectin levels caused by candesartan and temocapril may be related to the change in the M value.There have been2recent reports on the concentrations of adiponectin in patients with essential hypertension.16,17 Adamczak et al16reported that plasma adiponectin concen-trations were decreased in patients with essential hyperten-sion.In contrast,Mallamaci et al17showed that adiponectin levels were higher in hypertensive patients than in normoten-sive subjects and were inversely related to creatinine clear-ance in hypertensive patients and that creatinine clearance was the only independent predictor of adiponectin concentra-tions.It is possible that latent renal dysfunction had compli-cated essential hypertension in the latter study.Thus,results of recent studies on adiponectin in essential hypertension have been inconsistent.Our results showed that adiponectin concentrations were reduced in insulin-resistant essential hypertensives but not normotensives or non–insulin-resistantFuruhashi et al Adiponectin and Renin-Angiotensin System Blockade79hypertensives,suggesting that hypoadiponectinemia in essen-tial hypertensives is associated with insulin resistance. Adiponectin concentrations were not related to mean blood pressure in the present study.Contrary to this result,signif-icant negative correlations were found between plasma adi-ponectin concentration and mean,systolic,and diastolic blood pressures in33essential hypertensives and33normo-tensives.16Other studies,however,demonstrated that adi-ponectin levels were not related to blood pressure in180 overweight/obese Asian subjects35or in36hypertensive patients.17Moreover,another study showed that serum adi-ponectin levels were negatively correlated with systolic blood pressure and diastolic blood pressure in a large number of Japanese subjects(705men and262women),but these correlations were not significant after adjustment for age, gender,and BMI.36In animal studies,effects of recombinant adiponectin on body weight,glucose,and lipid metabolism have been clearly demonstrated.9,37,38However,its effect on blood pressure regulation has not been reported.The delin-eation of the relation between adiponectin and blood pressure requires more study.One limitation of this study is the small number of subjects enrolled.We demonstrated that serum adiponectin concentra-tions were gender-related,being higher in women than in men as previously reported.8,36Although there was no intergroup difference in gender in the present study,it is important to confirm our findings by studies with more patients.Further-more,studies with larger populations of subjects in whom various kinds of RAS blocking agents are used seem to be needed.In conclusion,our results suggest that hypoadiponectine-mia and disturbance of lipid metabolism are associated with insulin resistance in patients with essential hypertension and that RAS blockade increases serum adiponectin concentra-tions with improvement in insulin sensitivity. PerspectivesIt has been suggested that adiponectin modulates endothelial function and has an inhibitory effect on vascular smooth muscle cell proliferation.39,40Moreover,adiponectin has been shown to be accumulated in an injured artery from the plasma and to suppress macrophage-to-foam cell transformation in vitro and in vivo.10,41,42On the basis of these observations,it is possible that reduction in adiponectin concentrations may account,at least in part,for the higher incidence of athero-sclerotic diseases in essential hypertension and that RAS blockade may prevent,at least in part,atherosclerosis via increased adiponectin concentrations.Recent clinical trials,such as the Captopril Primary Pre-vention Project(CAPPP),43the Heart Outcomes Prevention Evaluation(HOPE),44and the Losartan Intervention For Endpoint reduction in hypertension study(LIFE),45suggest that RAS blockade may substantially lower the risk for type 2diabetes.One of the mechanisms underlying this effect may be an increase in adiponectin concentrations by RAS block-ade.The demonstration that RAS blockade increases adi-ponectin concentrations with improvement in insulin sensi-tivity might provide a scientific rationale for the use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers for the prevention of diabetes in high-risk hypertensive patients.References1.Scherer PE,Williams S,Fogliano M,Baldini G,Lodish HF.A novelserum protein similar to C1q,produced exclusively in adipocytes.J Biol Chem.1995;270:26746–26749.2.Maeda K,Okubo K,Shimomura I,Funahashi T,Matsuzawa Y,MatsubaraK.cDNA cloning and expression of a novel adipose specific collagen-like factor,apM1(AdiPose Most abundant Gene transcript1).Biochem Biophys Res Commun.1996;221:286–289.3.Hu E,Liang P,Spiegelman BM.AdipoQ is a novel adipose-specific genedysregulated in obesity.J Biol Chem.1996;271:10697–10703.4.Nakano Y,Tobe T,Choi-Miura NH,Mazda T,Tomita M.Isolation andcharacterization of GBP28,a novel gelatin-binding protein purified from human plasma.J Biochem(Tokyo).1996;120:803–812.5.Arita Y,Kihara S,Ouchi N,Takahashi M,Maeda K,Miyagawa J,HottaK,Shimomura I,Nakamura T,Miyaoka K,Kuriyama H,Nishida M, Yamashita S,Okubo K,Matsubara K,Muraguchi M,Ohmoto Y, Funahashi T,Matsuzawa Y.Paradoxical decrease of an adipose-specific protein,adiponectin,in obesity.Biochem Biophys Res Commun.1999;257:79–83.6.Ouchi N,Kihara S,Arita Y,Maeda K,Kuriyama H,Okamoto Y,HottaK,Nishida M,Takahashi M,Nakamura T,Yamashita S,Funahashi T, Matsuzawa Y.Novel modulator for endothelial adhesion molecules: adipocyte-derived plasma protein adiponectin.Circulation.1999;100: 2473–2476.7.Weyer C,Funahashi T,Tanaka S,Hotta K,Matsuzawa Y,Pratley RE,Tataranni PA.Hypoadiponectinemia in obesity and type2diabetes:close association with insulin resistance and hyperinsulinemia.J Clin Endo-crinol Metab.2001;86:1930–1935.8.Hotta K,Funahashi T,Arita Y,Takahashi M,Matsuda M,Okamoto Y,Iwahashi H,Kuriyama H,Ouchi N,Maeda K,Nishida M,Kihara S,Sakai N,Nakajima T,Hasegawa K,Muraguchi M,Ohmoto Y,Nakamura T, Yamashita S,Hanafusa T,Matsuzawa Y.Plasma concentrations of a novel,adipose-specific protein,adiponectin,in type2diabetic patients.Arterioscler Thromb Vasc Biol.2000;20:1595–1599.9.Yamauchi T,Kamon J,Waki H,Terauchi Y,Kubota N,Hara K,Mori Y,Ide T,Murakami K,Tsuboyama-Kasaoka N,Ezaki O,Akanuma Y, Gavrilova O,Vinson C,Reitman ML,Kagechika H,Shudo K,Yoda M, Nakano Y,Tobe K,Nagai R,Kimura S,Tomita M,Froguel P,Kadowaki T.The fat-derived hormone adiponectin reverses insulin resistance asso-ciated with both lipoatrophy and obesity.Nat Med.2001;7:941–946. 10.Okamoto Y,Kihara S,Ouchi N,Nishida M,Arita Y,Kumada M,OhashiK,Sakai N,Shimomura I,Kobayashi H,Terasaka N,Inaba T,Funahashi T,Matsuzawa Y.Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice.Circulation.2002;106:2767–2770.11.Maeda N,Takahashi M,Funahashi T,Kihara S,Nishizawa H,Kishida K,Nagaretani H,Matsuda M,Komuro R,Ouchi N,Kuriyama H,Hotta K, Nakamura T,Shimomura I,Matsuzawa Y.PPAR␥ligands increase expression and plasma concentrations of adiponectin,an adipose-derived protein.Diabetes.2001;50:2094–2099.12.Yang WS,Jeng CY,Wu TJ,Tanaka S,Funahashi T,Matsuzawa Y,WangJP,Chen CL,Tai TY,Chuang LM.Synthetic peroxisome proliferator-activated receptor-␥agonist,rosiglitazone,increases plasma levels of adiponectin in type2diabetic patients.Diabetes Care.2002;25:376–380.bs TP,Wagner JA,Berger J,Doebber T,Wang WJ,Zhang BB,Tanen M,Berg AH,O’Rahilly S,Savage DB,Chatterjee K,Weiss S, Larson PJ,Gottesdiener KM,Gertz BJ,Charron MJ,Scherer PE,Moller DE.Induction of adipocyte complement-related protein of30kilodaltons by PPAR␥agonists:a potential mechanism of insulin sensitization.Endo-crinology.2002;143:998–1007.14.Lind L,Berne C,Lithell H.Prevalence of insulin resistance in essentialhypertension.J Hypertens.1995;13:1457–1462.15.Iimura O.Insulin resistance and hypertension in Japanese.Hypertens Res.1996;19(suppl1):S1–S8.16.Adamczak M,Wiecedil;cek A,Funahashi T,Chudek J,Kokot F,MatsuzawaY.Decreased plasma adiponectin concentration in patients with essential hypertension.Am J Hypertens.2003;16:72–75.17.Mallamaci F,Zoccali C,Cuzzola F,Tripepi G,Cutrupi S,Parlongo S,Tanaka S,Ouchi N,Kihara S,Funahashi T,Matsuzawa Y.Adiponectin in essential hypertension.J Nephrol.2002;15:507–511.18.Miyazaki Y,Murakami H,Hirata A,Fukuoka M,Masuda A,Ura N,Shimamoto K.Effects of the angiotensin converting enzyme inhibitor80Hypertension July2003。

原发性高血压

2
• 三高： • 患病率高：1991年患病率为11.88％，患病人数 9000万；1998年为1.1亿，平均每11人或每3个家庭有一名高血压患者。 • 致残率高：目前我国有脑卒中患者600万，其中 75％不同程度丧失劳动力，40％重度致残；每年有150万人新发脑卒中。 • 死亡率高：心脑血管病占我国城市人口死亡因素构成原因的41％，这个数字在北京已达51％。 • 三低： • 知晓率低：1991年调查表明，对高血压的知晓率城市为36.3％，农村为13.7％。 • 服药率低：城市17.4％，农村5.4％。 • 控制率低：血压控制到140／90mmHg以下者，城市4.2％，农村0.9％。
原发性高血压
钟祥市中医院心病科左璐
1
• 原发性高血压(essential hypertension,EH)，又称高血压病，是常见的心血管疾病之一，也是世界上历史悠久、流行最广、危害最重、隐蔽最深的一种心血管疾病，与人类死亡的主要疾病如冠心病、脑血管疾病等密切相关。发病率高、致残率高、死亡率高，而知晓率低、治疗率低、控制率低。因此，世界各国均十分重视原发性高血压从发病机理致临床防治的研究。
• • • • 评估高血压患者从以下几个方面着手： ①并存的其它心血管危险因素； ②靶器官损害； ③并存临床情况如心，脑血管病，肾病及糖尿病； • ④ 患者个人情况及经济条件等。 Nhomakorabea18
高血压的危险分层
血 1级高血压低危中危高危极高危压 2级高血压中危中危高危极高危
存在的危险因素情况无其它危险因素 1～2个危险因素＞3个危险因素或靶器官损害或糖尿病并存有其它临床情况
14
五、诊断与鉴别诊断
• (一)诊断 • 1．确诊高血压，即血压是否确实高于正常，达到高血压诊断标准。P133。 • 2．原发性高血压分级、分层 • 1999年以前WHO标准，确诊高血压后，可按临床表现分为3期，3个时期的共同点就是血压已达到确诊高血压的水平。 • 1999年WHO/ISH高血压指南不再将原发性高血压分期，而是综合原发性高血压患者血压水平、靶器官损害、并发症及危险因素，将原发性高血压低危、中危、高危和极高危4种程度。

文献检索操作试题及答案

一、CBMweb1．基本检索：砷中毒流行病学方面的文献2．主题检索：砷中毒流行病学方面的文献3．主题词不扩展不加权检索白血病诊断方面的文献4. 主题词扩展加权检索白血病诊断方面的文献5．分类途径：病毒性肝炎病因学方面的文献6. 分类途径：高血压与脑血管疾病的关系先分类检索高血压，再分类检索脑血管疾病，再在检索历史中合并。

7．查找解放军总医院的叶平作为第一作者发表的文章。

基本检索8．查找温州医学院学报的创刊年份以及本刊上发表的有关呼吸衰竭的文献期刊检索、《PubMed》/PubMed 1．基本检索：肺癌和吸烟关系的文献lung cancer，smoke ，smoking，smoked（用截词符*）2．检索2007年以来2岁（即出生至23个月）小儿哮喘的综述文献（asthma，review），并将前两条存储到剪贴板。

3．检索作者为Black，且标题中有Hypertension的文献。

4．主题数据库（Mesh Database）检索：艾滋病（AIDS）预防和控制（Prevention and Control）5．期刊数据库（Journals Database）检索：PubMed中收录关于视力测定(Optometry)的期刊有哪些？Advanced-juurnals6．引文匹配器（Single Citation Matcher）Hepatology，2000，32（3）：6787．找出肾性高血压（renal hypertension）的主题词，以及其上位主题词和下位主题词。

六、SD()1、找出刊名中有验光(Optometry)的杂志，并写出它们的ISSN号。

Search2、找出护理和保健专业(Nursing and Health Professions)07年7-9月最热门的25篇论文，其中被引用次数最多的一篇论文共被引用了多少次，抄下该篇论文的信息。

被引用最多：3、2008年以后发表的关于原发性高血压(primary hypertension、essential hypertension、spontaneous hypertension)病理学(pathology、pathologic...)研究的文献。

神经内科常用英文词汇

神经内科常用英文词汇AAbadie's Sign 阿巴迪征(跟腱受压无感觉，见于脊髓痨) Abaptiston 安全开颅圆锯abarognosis 压觉缺失abasia astasia 立行不能abasia 步行不能abdominal reflex 腹壁反射abduction 外展abiotrophy 生活力缺失ablepsia 视觉缺失ablute 切除abnormal 异常abnormity 畸形abrupt 意外absolute hemianopia 完全偏盲abstinent 戒断症状abstraction 抽象acalculia 失算acataleptic 智能缺陷acatamathesia 理解不能acataphasia 连贯表达不能acatastasia 反常acathexis 心力贯注不能acathisia 静坐不能accessory cramp 痉挛性斜颈accommodation reflex 调节反射accommodation 适应aceburtolol 醋丁洛尔acedia 淡漠性忧郁症acenesthsia 存在觉缺失acenocoumarol 新抗凝acephalia 无头畸形acervulus 松果体石acetazolamide 乙酰唑胺acetohrdroxamic acid 乙酰氧肟酸acetophenazine乙酰非那嗪acetylcholinergic pathway 乙酰胆碱能通路acetylcholinesterase 乙酰胆碱脂酶acetylcholine 乙酰胆碱acetylglutamide 乙酰谷氨酰胺acetylsalicylic acid 乙酰水杨酸acetyl-spiramycin 乙酰螺旋霉素Achilles jerk 踝反射Achilles tendon reflex 踝反射acinesia 运动不能aconative 意向缺失acorea 无瞳孔acouesthesia 听觉acousmatamnesia 听觉性健忘acousma 幼听acoustic neuroma 听神经瘤acoustic pathway 听觉传导路acoustic stria 听纹acouticolateral area 听侧线区acroagnosis 肢体感觉缺失acroanesthesia 肢端麻木acrobrachycephaly 扁头acrocephalosyndactyly 尖头并指acrocephaly 尖头acrocinesis 运动过多acrodynia 肢体疼痛症acrognosis 肢体感acrokinesia 感觉过敏acrokinesis 运动过多acromegaly 肢体肥大症acroneurosis 肢体神经官能症acroparalysia 肢麻痹acroparesthesia 肢体感觉异常acrosclerosis 肢体硬化症acrotrophoneurosis 四肢营养神经病actinine 辅肌动蛋白actinomycosis of brain 脑放线菌病actinoneuritis 放射性神经炎actin 肌动蛋白action tremor 动作性震颤active negativism 主动违拗症actomyosin 肌动球蛋白acuity 敏度acute alcohol intoxication 急性酒精中毒acute brain syndrome 急性脑综合征acute poliomyelites 急性脊髓前角灰质炎acute spontaenous myelites 急性非特异脊髓炎acute suppurative myelites 急性化脓性脊髓炎acyclovir 无环鸟苷acystinervia 膀胱神经无力Adamkiewicz's demilunes 阿达姆基维支新月形细胞(在有髓神经纤维的神经膜底下) adaptation 适应adduction 内收adenoma of pituitary gland 脑下垂体腺瘤adenovirus 腺病毒adiphenine 解痉素adiposis cerebralis 脑性肥胖症adiposis dolorosa 痛性肥胖症adrenergic 肾上腺素能adreno leukodystrophy 脑白质营养不良aerasthenia 飞行员精神衰弱aetiology 病因学affektepilepsie 情感性痉挛affensplate 月状沟(大脑枕叶)afferent 传入African meningitis 非洲脑膜炎(昏睡病) aganglionosis 神经节细胞缺乏症ageing of nervous tissue 神经组织老化agenesis of corpus callosum 胼胝体发育不良agitation 焦虑agnosia 失认agraphia 失写agyria 无脑回akathisia 静坐不能akinesia 运动不能akinetic seizures 运动不能发作akinetic-rigid syndrome 运动不能-强直综合征Akureyri disease 良性肌痛性脑脊髓炎alar plate 翼板albendazole 阿苯达唑alcoholic coma 酒精中毒性昏迷aldosterone 醛固酮alertness 警觉alexia 失读alleviated 缓和allopurinol 别嘌呤醇allucination 幻觉almufibrate 氯贝丁酯铝alprenollol 心得舒alptazolam 阿普唑仑alternating hemiplegia 交替性偏瘫altitudinal hemianopia 上下性偏盲aluminium nicotinate 烟酸铝Alzheimer's disease 阿尔塞梅茨病amantadine 金刚烷胺amaurotic idiocy 黑朦性白痴amaurotic 黑朦ambient cistern 环池amblyopic 弱视ameboid glia 阿米巴样神经胶质细胞ameliorate 改善amentia 精神错乱amiculum of olive 橄榄核囊amikacin 丁胺卡那霉素aminoacidurias 氨基酸尿aminocaproic acid, EACA 6-氨基己酸aminopyridine 氨基比林amitriptyline 阿米替林amnesic 遗忘amobarbital 异戊巴比妥amoxycillin 羟氨苄青霉素amphetamine 苯丙胺amphetamines 安非他命amplitude 幅度amyotonia congenita 先天性肌张力不全症amyotrophia 肌萎缩amyotrophic lateral sclerosis 肌萎缩性侧束硬化症anaerobic 厌氧的anal reflex 肛门反射analgesia 痛觉缺失anencephaly 无脑anesthesia dolorosa 痛性感觉缺失anesthesia 感觉缺失aneurysms 微动脉瘤aneuryson 动脉瘤angiography 血管造影angular gyrus 角回anisocoria 瞳孔不等大ankylosing spondylitis 关节固定性脊柱炎anorexic 厌食anosmia 嗅觉缺失anosognosia 病觉缺失anosognosia 偏瘫否认ansamysin 襻霉素anterior amygdaloid 前杏仁区anterior cerebellar incesure 小脑前切迹anterior commissure 前连合anterior corticospinal tract 皮质脊髓前束anterior fontanel 前囟anterior horn of lateral ventricle 侧脑室前角anterior lateral suleus 前外侧沟anterior limb of internal capsule 内囊前脚anterior median fissure 前正中裂anterior medullary velum 前髓帆anterior parolfactory suleus 前旁嗅沟anterior perforated substania 前穿质anterior speech cortex 前说话区(Broca氏区) anterior spinocerebellar tract 脊髓小脑前束anterior white commissure 白质前连合anterior 前anterior(ventral) funiculus 前索(脊髓)anterior(ventral) horn 前角(脊髓)anterior(ventral) root 前根anterograde amnesia 顺行性遗忘anterograde axoplasmic transport 顺向轴浆输送anterograde degeneration 顺行变性anterolateral corticospinal tract前外侧皮质脊髓束anterolateral 前外侧anterolivary suleus 橄榄前沟antiepilepsirin 抗癫灵anxiety hysteria 焦虑性癔病anxiety tension state 焦虑紧张状态anxiety 焦虑症aone of Obersteiner?Redlich 奥贝斯坦纳?热里希氏带Apert syndrome 塔头并指畸形症aphasia 失语aphingolipid 神经鞘脂apnoea 窒息apoplectic coma 中风性昏迷apraxia 失用aprotinin 抑肽酶arachnoid granulation 蛛网膜颗粒arachnoid villi 蛛网膜绒毛arachnoid 蛛网膜arachnoiditis 蛛网膜炎archeo cerebellum 古小脑arcuocerebellar fibers弓状小脑纤维area postrema 最后区area temporalis inferior 颞下区area temporalis media 颞中区area temporalis superior 颞上区area temporalis transverse externa 颞横外侧区area temporalis transverse interna 颞横内侧区area 区areflexia 反射消失arfonad 咪噻芬arginine 精氨酸Arnold-Chiari malformation 先天性小脑延髓下疝畸形arteriovenous malformation of brain 脑动静脉畸形arteriovenous malformotion 动静脉畸形arthroneuralgia关节神经痛articulation 连接ascending reticular activing system 网状上行激活系统ascending reticular inhibiting system 网状上行抑制系统assessment 评估association neuron联络神经元astereognosia 立体觉失认asterixis 扑翼样震颤asthenia 衰弱asthenic syndrome 脑衰弱综合征asthenocoria 瞳孔反应迟钝astrocytoma 星形细胞瘤astroglia cell 星形胶质细胞asymmetrical synapse 不对称型突触asymmetry 不对称asymptomatic 无症状asynchronism 协调障碍asyndesis 言语不能asynergy 协同不能asystole 心脏停搏atactic 协调不能atactiform 共济失调样ataxia 共济失调atelocephalous 头发育不全atelocephaly头颅发育不全atenolol 阿替洛尔athalposis 温觉缺失atheroma 粥样斑atherosclerosis 动脉硬化athetosis 手足徐动症atlanto-axial subluxation 寰枢椎半脱位atonia 肌张力缺失atonic bladder 无张力性膀胱atopognosia 位置觉缺失atremia 歇斯底里性步行不能atretopsia 瞳孔闭锁atypical absences 非典型发作atypical 非典型auditory evoked potential 听觉诱发电位auditory hallucination 幻听auditory radiation 听辐射aural nystagmus 耳原性眼球震颤aural vertigo 耳源性眩晕aura先兆automatism 自动症autonomic nervous system 自主神经系autonomous bladder 自主性膀胱autonomous neurogenic bladder 自主神经原性膀胱autosomal 常染色体autotomography 自体感知不能autotophagnosia 自体结构失认Avellis' Syndrome 阿费利斯综合征(疑核脊髓丘脑性麻痹) avulsion of scalp 头皮撕裂伤axis 枢椎axo-axonal synapse 轴-轴突触axo-dendritic synapse 轴-树突触axolemma 轴膜axon hillock 轴丘axonotmesis 轴突中断axon 轴突axophage 噬髓鞘细胞axoplasmic flow 轴浆流axoplasmic transport 轴浆输送axopodium 轴伪足axo-somatic synapse 轴-体突触axosopongium 轴突海绵质axo-spinous synapse 轴-棘突触Ayala's index 阿亚拉指数(脑脊液压指数)Ayer's test 艾尔试验(检测椎管阻滞)aypnia 失眠azathioprine 硫唑嘌呤azidothymidine, AZT 叠氮胸苷BBabinski sign 巴彬斯基征Babinski-Nageotte syndrome 延髓腹外侧综合征Backer muscular dystrophy 贝克肌营养不良backward progression 后退步态baclofen 氯苯氨丁酸Baillarger's line 贝亚尔若线(大脑皮层锥体细胞层内的白色带)Balint syndrome 巴林特综合征(双侧顶－枕区损害)ballismus 投掷症Balo disease 巴娄病 (同心层型轴周性脑炎)band of Kaes?Bechterew 卡依斯?贝克特如氏带Barany's pointing test 巴腊尼指向试验(检脑损害)Barany's symptom 巴腊尼症状(冷热水试验)barbitalism 巴比妥中毒Bard's sign 巴尔德征(眼球震颤征)Barre-Guillain Syndrome 急性热病性多神经炎Barre-Lieou Syndrome 后颈交感神经综合征barrier 屏障baryencephalia 智力迟钝baryesthesia 压觉baryglossia 言语拙笨barylalia 言语不清basal plate 基板basiarachnitis 颅底蛛网膜炎basicranial 颅底basilar cistern 基底池basilar fracture 颅底骨折basilar impression 颅底凹陷basilar invagination 颅底陷入症basilar sinus 基底窦basilar suleus 基底沟basinasial 颅底鼻根的basioccipital 枕骨底部的basis pontis 基底部(脑桥)basophil 嗜碱性细胞Bassen-Kornzweig syndrome 棘状红细胞－β－脂蛋白缺乏症Bastian-Bruns Sign 巴斯欣-布伦斯征(从头部到腰膨大部的脊髓有完全横贯性损害,下肢键反射就消失)bathrocephaly 梯头bathyanesthesia 深部感觉缺失bathyesthesia 深部感觉bathyhyperesthesia 深部感觉过敏bathyhypesthesia 深部感觉迟钝Batten-Mayou disease 少年型黑蒙性白痴Bayle's disease 贝尔病(精神错乱者的进行性全身性麻痹)Beale's ganglion cells 比尔神经节细胞(双极细胞)Beard's disease 神经衰弱Behcet syndrome 白塞综合征Bekhterev's layer 别赫捷列夫层(大脑皮层外粒层的纤维层)Bekhterev's nucleus 别赫捷列夫核(前庭神经上核)Bekhterev's reaction 别赫捷列夫反应Bekhterev's reflex 别赫捷列夫反射(深层反射;腹下部反射;瞳孔反射;鼻反射) Bekhterev's symptom 别赫捷列夫症状(面肌麻痹)Bekhterev's test 别赫捷列夫试验(检坐骨神经痛)Bell's law 贝尔定律(脊髓神经前根为运动根,后根为感觉根)Bell's mania 急性谵妄Bell's nerve 胸长神经Bell's palsy 贝尔麻痹Bell's phenomenon 贝尔现象bemegride 美解眠benactyzine 胃复康Benedict's syndrome 中脑红核综合征Benedikt's syndrome 本尼迪克特综合征(一侧动眼神经麻痹,对侧运动过度,benign congenital hypotonia 良性先天性肌张力减低benign essential tremor 良性特发性震颤benign intracranial hypertension 良性颅高压benign myalgic encephalomyelitis 良性肌痛性脑脊髓炎benign paroxysmal vertigo 良性发作性眩晕benign positional vertigo 良性位置性眩晕benserazide 苄丝肼医学全在.线提供benspryzine 苯纳哌嗪benumb 使瘫痪benzathine 苄星青霉素benzhexol hydrochloride 盐酸苯海索benzhexol 苯海索(安坦)benztropine 苯甲托品benzylpencilline 苯唑青霉素Berger's paresthesia 贝格尔感觉异常(青少年的一侧或两侧下肢感觉异常,无力,但无他觉症状)Berger's sign 贝格尔征(不规则或椭圆性瞳孔,见于早期脊髓痨,麻痹性痴呆)Bergeron's chorea贝尔热隆病(电击样舞蹈病,激烈而有规律的痉挛,但为良性病程) Bergmann's cells 贝格曼细胞(小脑皮层分子层内的特殊神经胶质细胞)Bergmann's cords 第四脑室髓纹,听髓纹Bergmann's fibers 贝格曼纤维(从小脑皮层分子层放射并进入软脑膜的突)Beri-beri(thiamine deficiency) 硫胺(VitB1)缺乏症Bernhard's disease 感觉异常性股痛Bernheimer's fibers 伯恩海默纤维(自视神经束至柳氏体的一种脑神经纤维束) betahistine 培他啶bethanechal (-甲基氨甲酰胆碱Betz's cells 贝茨细胞Bezold's abscess 颞骨骨膜下脓肿Bezold's perforation 颞骨乳突内面穿孔Bezold's sign 贝措尔德征(乳突炎)Bezold's triad 贝措尔德三征(耳硬化)Bianchi's syndrome 比昂基综合征(一种感觉性失语症性综合征,伴失用症及失读症)Bichat's canal 大脑大静脉Bichat's fissure 大脑横裂Bichat's foramen 蛛网膜孔Bielschowsky disease 幼儿型家族性黑蒙性白痴Bielschowsky's method 比尔肖夫斯基法(论证神经轴突及网状纤维的氨银染法) Bielschowsky's-Jansky disease 晚期婴儿型家族性黑蒙性痴呆Biernacki's sign 别尔纳茨基征(脊髓痨及麻痹性痴呆时的尺神经瘫痪)bilateral hemianopia 双侧偏盲bilateral 双侧Billroth's disease比罗特征(假性脑(脊)膜突出)binocular hemianopia 双眼偏盲binocular microscope 双目显微镜Binswanger disease 宾斯万格病(皮质下脑病)biopsy 活检Biot's respiration 比奥呼吸(间歇性呼吸暂停,见于颅内压增高)bipolar neuron 双极神经元bitamporal 颞侧bitemporal hemianopia 颞侧偏盲bithionol 硫双二氯酚black-out syndrome 黑蒙综合征blackouts 黑朦bladder 膀胱blastoneuropore 胚神经孔blepharoptosis 睑下垂blepharospasm 睑痉挛blink reflex 瞬目反射blink 眨眼blood-brain barrier 血脑屏障blood-CSF barrier 血脑脊液屏障blood-nervus barrier 血神经屏障Blumenau's nucleus 布路门奥核(楔核外侧核)Blumenbach's clivus 布卢门巴赫斜坡(与枕骨底突相连的蝶骨斜坡) Blumenbach's process 筛骨钩突blurring 模糊body of lateral ventricle 侧脑室体部body, corpus, complex 体Bonnier's syndrome 邦尼埃综合征(前庭神经外侧核或前庭束损害)Bornholm disease 流行性肌痛Bourneville's disease 结节硬化症boutons en passant 旁结boutons terminaus 终结bouts 发作bowel 直肠boxing encephalopathy 拳击员脑炎brachcephaly 短头brachial plexus 臂丛brachium conjunctivum 结合臂brachium pontis 脑桥臂brachium 臂brachycranic 短颅的(颅指数为81.0至84.9)bradycardia 心动过缓bradykinesia 运动迟缓bradylalia 言语迟缓bradylexia 阅读过慢bradylogia 言语过慢bradyphemia 言语过慢bradyphrasia 迟语症bradyphrenia 智力迟钝(流行性乙型脑炎)bradypragia 动作过慢brain, encephalon 脑Brain's reflex 布雷恩反射(当病人采取四足位置时,偏瘫性屈曲上臂伸直) brainstem 脑干医.学全,在.线,提供briskly 活跃Brissaud's syndrome 交叉性面痉挛偏瘫综合征Broca's area 布若卡氏区Brodmann's areas 布劳德曼区(大脑皮层细胞结构分区)bromazepam 溴基安定bromazolam 宁神定bromocriptine 溴隐亭Brown-Sequard syndorme 脊髓半切综合征Brudzinski sign 布鲁金斯基征Bruns' syndrome 布伦斯综合征(第四脑室包囊虫眩晕综合征)Budge's center 布吉氏中枢Buerger disease 闭塞性血栓性脉管炎bufetolol 丁呋心安Buiswangen disease 缺血性白质脑病bulbar paralysis 球麻痹Burdach's columns 布尔达赫柱(脊髓楔束)Burdach's fasciculus 布尔达赫束(大脑上纵束)Burdach's fibers 布尔达赫纤维Burdach's fissure 布尔达赫裂(脑岛外侧面和岛盖内面间裂)Burdach's nucleus 布尔达赫核(楔束核)buspirone 丁螺环酮Ccabernous sinus 海绵窦cacesthesia 感觉异常cachinntion 癔病狂笑cafe au lait spots 咖啡牛乳色斑caffeine 咖啡因Caffey disease 婴儿骨皮质增生症Cajal's cells 卡哈尔细胞(星形胶质细胞)Cajal's double method 卡哈尔双重染色法(显示神经节细胞) Cajal's method 卡哈尔染色法(显示星形胶质细胞)calan 卡兰calcar avis 禽距calcarine fissure 距状裂calcified 钙化Calleja's islets 卡耶哈岛(海马回嗅觉小岛)callosal suleus 胼胝体沟callosum 胼胝体caloric nystagmus 温热性眼球震颤caloric test冷热试验Canavan disease 海绵状脑白质营养不良症candida 念珠菌canine hysteria 犬惊病canine spasm 痉笑caprylhydroxamic acid 辛酰氧肟酸capsule 囊carbamazepine 卡马西平carbechal 氨甲酰胆碱carbenicillin 羧苄青霉素carbidopa 卡比多巴cardiac plexus 心丛cardio-accelerating center心加速中枢cardio-encephalopathy 心性脑病cardio-inhibitor center 心抑制中枢cardioneurosis 神经性循环衰弱cardioplegia 心麻痹carotid angiograpathy 颈动脉血管造影carotid bifuracation 颈动脉分叉carotid compression 压颈动脉试验carotid sinus reflex 颈动脉窦反射carotid sinus syncope 颈动脉窦性晕厥carpal tunnel syndrome 腕管综合征carteolol 喹酮心安cartid-cavernous fistula 颈动脉海绵窦瘘caseating 干酪样cataplexy 猝倒catatonia 紧张症catatonic pupil 紧张性瞳孔catecholamine 儿茶酚胺categories 类型cauda equins 马尾(脊髓)causalgia 灼性神经痛cavernous sinus 海绵窦综合征cefadroxil 头孢拉定cefaloridine 头孢噻啶cefathiamidine 头孢硫脒celiac plexus 腹腔丛cellulitis 蜂窝织炎cenral spinal cord dyndrome 脊髓中央综合征center 中枢centers of autonomic nerve自主神经中枢central canal 中央管central core disease 中央轴突症central excitatory state 中枢兴奋状态central gray substance 中央灰质central pain 中枢性疼痛central sulcus 中央沟central suleus of insula 岛中央沟central tegmental tract 被盖中央束centraphose 中枢性暗觉centrifuged deposit 离心后沉淀centrokinesia 中枢性运动cephalgia 头痛cephalic flexure 头曲cephalin 脑磷脂cephalitis 脑炎cephalocele 脑膨出cephalocentesis 头颅穿刺术cephalochord 头索cephalodynia 头痛cephaloplegia 头面肌瘫痪cephalothin sodium 头孢噻吩钠cephaoexin 头孢氨苄cephazolin sodium 头孢唑啉钠ceptriaxone 头孢噻肟二嗪ceramidase 神经鞘氨醇酶ceramide glucoside 葡糖脑苷脂ceramide trihexoside 神经鞘氨醇己三糖苷ceramide 神经鞘氨醇cerebellar ataxia 小脑共济失调cerebellar atrophy 小脑萎缩cerebellar corpus 小脑体cerebellar cortex 小脑皮质cerebellar ectopia 小脑外疝cerebellar hemisphere syndrome 小脑半球综合征cerebellar hemisphere 小脑半球cerebellar plate 小脑板cerebellar pressure cone 小脑压迫圆锥cerebellar tonsillar herniation 小脑扁桃体疝cerebellitis 小脑炎cerebello- olivary fibers小脑橄榄纤维cerebellomedullary cistern 小脑延髓池cerebellopontine angle 小脑桥脑角cerebelloreticular fibers 小脑网状纤维cerebellorubral fibers 小脑红核纤维cerebellovestibular fibers 小脑前庭纤维cerebellum 小脑cerebral abscess 脑脓肿cerebral agenesis 大脑发育不全cerebral angiograpathy 脑血管造影cerebral atrophy 大脑萎缩cerebral commissure 大脑连合cerebral contusion 脑挫伤cerebral cortex 大脑皮质cerebral cysticercosis 脑囊虫病cerebral diaplegia 脑性双侧瘫痪cerebral dysgenesis 脑发育障碍cerebral edema 脑水肿cerebral embolism 脑栓塞cerebral haemorrhage 脑出血cerebral hemisphere 大脑半球cerebral infarction 脑梗死cerebral ischemia 脑缺血cerebral lipidosis 脑脂质增多症cerebral malacia 脑软化cerebral paragonimiasis 脑型肺吸虫病cerebral peduncle 大脑脚cerebral plasy 脑性瘫痪cerebral schistosomiasis 脑型血吸虫病cerebral sclerosis 脑硬化症cerebral spasm 大脑性痉挛cerebral thrombosis 脑血栓形成cerebral-arteriosclerotic dementia 脑动脉硬化性痴呆cerebriform 脑形的cerebritis 脑炎cerebrocuprein 脑铜蛋白cerebrogalactose 脑半乳糖cerebrogalactoside 脑半乳糖苷脂cerebrohyphoid 脑组织样的cerebroid 脑形的cerebrolysin 脑活素cerebroma 脑瘤cerebromacular degeneration 大脑黄斑变性症cerebromalacia 脑软化cerebromeningitis 脑膜脑炎cerebron 羟脑苷脂cerebropathy 脑病cerebrosclerosis 脑硬化cerebrose 脑半乳糖cerebroside 脑苷脂类cerebrosidosis 脑苷脂沉积病cerebrosis 脑病cerebrospinal fluid 脑脊液cerebrospinal leak 脑脊液漏cerebrospinal rhinorrhea 脑脊液鼻漏cerebrospinase 脑脊液氧化酶cerebrovascular accident 脑血管意外cerebrum 大脑医学全.在线网.站.提供ceroid 蜡样质ceruloplasmin 血浆铜蓝蛋白cervical ansa 颈袢cervical enlargement 颈膨大(脊髓)cervical flexure 颈曲cervical plexus 颈丛cervical rib syndrome 颈肋综合征cervical rigidity 颈强直cervical spondylosis 颈关节强直cervical vertigo 颈性眩晕cervical 颈的Cestan-Chenais syndrome 副－舌下神经麻痹综合征Chaddoch sign 查多克征Chamberlain's line 硬腭枕大孔(张伯伦)线Charcot's foot 夏科氏足(脊髓痨性关节病患者的畸形足)Charcot's gait 夏科氏步态(家族性共济失调步态)Charcot's joint 夏科氏关节(神经原性关节病)Charcot's syndrome夏科氏综合征(肌萎缩性侧索硬化,间歇性跛行,肝病性间歇热) Charcot's triad 夏科氏三征(眼球震颤,意向震颤,断音言语见于多发性硬化症)Charcot-Marie-Tooth disease 腓骨肌萎缩征Chassalgnac's tubercle 夏桑亚克结节(第六颈椎横突的颈动脉结节)chemical synapse 化学突触Cheyne-Stokes nystagmus 节律性眼球震颤chiasmatic cistern 交叉池childhood dystrophy 儿童营养不良chitoneure 神经膜鞘chlomezanone 芬那露chloral hydrate 水合氯醛chloramphenicol 氯霉素chlorazepate 二钾氯氮卓chloridiazepoxide 利眠宁chlorimipramine 氯丙咪嗪chlormezanone 氯苯甲酮chloroquine 氯喹chlorpromazine 氯丙嗪chlorprothixene 泰尔登chlorthialidone 氯噻酮chocking 窒息cholesteatom 胆脂瘤cholestipol 降胆宁cholestyramine 消胆胺考来烯胺cholinergic 胆碱能cholinesterase 胆碱脂酶cholinolytic 抗胆碱cholinomimetic 类胆碱chondroitine 硫酸软骨素chorda tympani 鼓索支chordiazepoxide 氯氮平chordoma 脊索瘤chorea 舞蹈病choreiform 舞蹈病样的choreoathetosis 舞蹈手足徐动症choroid epithelium 脉络丛上皮choroid fissure 脉络裂choroid plexus of fourth ventricle 第四脑室脉络丛choroid plexus of lateral ventricle 侧脑室脉络丛choroid plexus of third ventricle 第三脑室脉络丛choroid plexus 脉络丛choroid 脉络膜chromidial substance 嗜染质chromphil substance 染色质chronic progressive inflammatory polyneuropathy 慢性进行性炎症性多发性神经病chronotaraxia 定时不能Chyne-Stokes respiration 潮式呼吸ciliary medullary center 延髓睫状体中枢ciliospinal center 睫脊中枢cillary neuragia 睫状神经痛cimetidine 西米替丁(甲氰咪呱)cinerea 灰质cingulate gyrus 扣带回cingulate suleus 扣带沟cingulectomy 扣带回切除术cingulumotomy 扣带回切开术cinnarizine 脑益嗪 (肉桂苯哌嗪)circle of Willis 脑底动脉环circumventricular organ 室周器cis-platinum 顺铂cistern 池cisternal puncture 小脑延髓池穿刺Clarke's cells 克拉克细胞(脊髓背核色素细胞)clasmatodendrosis 星形胶质细胞突破折clasp knife phenomenon 折刀现象clasp-knife 折刀样Claude's hyperkinesis sign 克洛德运动增强征(疼痛刺激时瘫痪肌肉的反射性动作) Claude's syndrome 克洛德综合征(一侧动眼神经瘫痪,对侧协同不能,讷吃)claw-hand 爪形手clindamycin 克林霉素clomipramine 氯丙咪嗪clonazepam 氯硝安定clonic seizure 阵挛发作clonic spasm 阵挛性痉挛clonidine 氯压定clonus 阵挛cloxacillin 邻氯青霉素coccidioidomycosis of brain 脑隐球菌病coccygeal 尾的cochlear duct 蜗管cochlear 迷路cochleostapedial reflex 镫骨肌反射coenzyme A 辅酶-Acoffin formation 柩状形成(神经细胞被吞噬)cogwheel rigidity 齿轮样强直Cohnheim's areas 孔海姆区(肌原纤维的多边形暗区)coiling reflex 蟠曲反射collateral eminence 侧副隆起collateral suleus 侧副沟collateral trigone 侧副三角Collet-Sicard syndrome 颅底综合征colliculocochleunuclear projection 下丘蜗核投射colliculo-olivary projection 下丘上橄榄投射colliculus 丘coma 昏迷comatose 昏迷commissure of inferior colliculus 下丘连合commissure 连合communicating hydrocephalus交通性脑积水compensate代偿compound microscope 复式显微镜compression of the brain 脑受压compression 压迫concha of cranium 颅盖concussion of brain 脑震荡concussion of spinal cord 脊髓震荡concussional 震荡Cone test 脑脊液动力检查confluence of sinus 窦汇congenital myopathy 先天性肌病congenital 先天性congruous hemianopia 同侧偏盲conjugate 共轭conjunctival reflex 结膜反射consciousness 意识consensual reflex 间接光反射consensual 间接constipation 便秘constitutional 原发性contraiadicate 禁忌contralateral 对侧contrecoup injury 对冲性损害contusion of spinal cord 脊髓挫伤contusion 挫伤conus medullaris 圆锥(脊髓)convalescent 恢复convergence defect 会聚障碍convergence spasm 会聚痉挛conversion hysteria 转换性癔病convuision 惊厥coordination 协调coprolalia 秽语症cornea 角膜corneal reflex 角膜反射cornucopia 外侧隐窝(第四脑室)corona radiation 辐射冠coronal 冠状的corpus callosum 胼胝体corpus Luysi 路易斯氏体corpus quadrigemina 四叠体corpus straitum 纹状体corssed hemianopia 异侧偏盲cortex 皮质Corti's arch 蜗螺旋神经节corticectomy 脑皮层切除术cortico- olivary fibers 皮质橄榄纤维corticobulbar tract 皮质脑干束corticocerebral 大脑皮层的corticocollicular projection 皮质下丘投射corticonuclear tract 皮质核束corticopontine tract 皮质脑桥束corticoreticular fibers 皮质网状纤维corticostriatal fibers 皮质纹状体纤维cortico-striato-spinal degeneration 皮质－纹状体－脊髓变性corticothalamic fibers 皮质丘脑纤维cortitectal fibers 皮质顶盖纤维cortival venous thrombophlebitis 皮质静脉血栓性静脉炎cough syncope 咳嗽晕厥coxsackie virus 柯萨奇病毒cramp 痛性痉挛cranial fontanel 颅囟医学.全在线cranial neuralgia 脑神经痛cranical meningocele 脑膜膨出craniectomy 颅骨切除术craniocele 脑膨出craniopharyngioma 颅咽管瘤craniopuncture 颅穿刺术craniorachischisis 颅脊柱裂cranioschisis 颅裂craniosclerosis 颅骨硬化craniostenosis 颅狭小craniostosis 颅缝骨化craniosynostosis 颅骨早期融合craniosynostosis 颅缝早闭craniotabes 颅骨软化craniotome 开颅器craniotomy 颅骨切开术craniotonoscopy 颅叩听诊法craniotopography 颅脑局部解剖学craniotrympanic 颅骨环锯术creatine kinase 肌酸激酶cremasteric reflex 提睾反射cretinism 呆小病Creutzfeld-Jacob disease 海绵状脑病cribriform 筛板cricothyroid 环甲crista ampullaris 壶腹嵴crossed paralysis 交叉性瘫痪cross-legged progression 交叉步态Crouzon syndrome 颅骨纤维结构不良综合征crucifixion attitude 十字架姿势(癔症性癫痫) cryptocalcarine gyrus 距状隐回cryptococcal 隐球菌的cryptogenic 原因不明cryptoglioma 隐期神经胶质瘤cryptoneurous 隐性神经系统的CSF-brain barrier 脑脊液脑屏障CSOM: chronic suppurative otitis media 慢性化脓性中耳炎culmen 山顶(小脑)cuneatocerebellar fibers 楔小脑纤维cuneocerebellar tract 楔小脑束Cushing disease 柯兴病cutancous 皮肤的cyanosis发绀cyclandelate 环扁桃酯cyclizine 苯甲嗪cyclobarbital 环巴比妥cyclohexanehexol 肌醇cyclophosphamide 环磷酰胺cycloserine 环丝氨酸cyclosprine 环孢菌素cycrimine 环戊丙醇cylindraxile 轴突cystic medial necrosis 囊性中央坏死cysticercosis 囊虫病cytarabine 阿糖胞苷cytidine diphosphate 胞二磷胆碱cytomegalovirus 巨细胞病毒cytopathy 细胞变性cytoplasmic glia 原浆性神经胶质细胞cytosine 胞嘧啶DDaCosta's disease 神经性循环衰弱dancing spasm 痉跳病Dandy-Walker syndrome 第四脑室闭锁综合征dapsome 氨苯砜dark degeneration 暗变性dark-field microscope 暗视野显微镜Darkshevich's fibers 达克谢维奇纤维Darkshevich'snucleus 达克谢维奇核(在中脑水管和第三脑室交界处) Daubenton's angle 多邦通角(枕角)Daubenton's line 多邦通线(由颅后点至颅底点的线)Daubenton's plane 多邦通平面(通过颅后点及眶下缘的平面) deafferentate 传入神经阻滞decerebrate rigidity 去大脑僵直decerebrate 去大脑declive 山坡(小脑)decorticate rigidity去皮层强直decubitus褥疮decussation of medial lemniscus 内侧丘系交叉decussation of superior cerebellar peduncle 小脑上脚交叉decussation 交叉deformity 畸形degeneration 变性Dejerine onion skin syndrome 代热林洋葱皮样综合征Dejerine's sign 代热林征(腹压加大时神经根炎症状加重)Dejerine's syndrome 代热林综合征Dejerine-Klumpke paralysis 下臂丛麻痹Dejerine-Landouzy dystrophy 代热林-兰杜茨营养不良Dejerine-Roussy syndrome 丘脑综合征Dejerine-Sottas syndrome 肥大性间质性多发性神经病delirium 谵妄delusion 妄想dementia 痴呆demyelinating 脱髓鞘dendritic spine 树突棘dendro-axonic synapse 树-轴突触dendro-dendrite synapse 树-树突触dendron 树突dendrophagocytosis 噬胞突作用dendro-somatic synapse 树-体突触denervation 去神经支配Denny-Brown neuropathy 遗传性感觉神经根神经病dentata 枢椎dentate gyrus 齿状回dentato rubral atrophy 齿状核红核萎缩deoxyribonucleic acid(DNA) 脱氧核糖核酸deprenyl 盐酸司立吉林depressor center 减压中枢Dercum disease 痛性肥胖症derencephalocele 颈椎脑突出dermatomal 皮区dermatomyositis 皮肌炎dermoid cyst 皮样囊肿descending pathway in auditory system 听觉系的下行通路desipramine 去甲丙咪嗪desoxyphenobarbital 扑痫酮医学全.在线.网.站.提供deviation 偏瘫Devic disease 视神经脊髓炎dexamethasone 地塞米松dextran-40 低分子右旋糖酐dextren sulfate 糖酐酯dextroamphetamine 右旋苯异丙胺diabetes insipidus 尿崩症diabetic amyotrophy 糖尿病性肌萎缩diabetic coma 糖尿病性昏迷diabetic neuritis 糖尿病性神经炎diacele 第三脑室diaclast 穿颅器diadochokinesia 轮替运动diagonal bundle 斜角带Diamox 乙酰唑胺diaphragma sellae 鞍隔diastematocrania 颅纵裂diastematomyelia 脊髓纵裂diataxia 两侧共济失调diazaepam 安定diazoxide 氯苯甲噻二嗪dicoumarin 双香豆素diencephalon 间脑diethylstilbestrol 乙烯雌酚difenidol 眩晕停diffuse sclerosis 弥漫性硬化dihydroergotoxin 氢化麦角碱dilated 扩张diltiazem 地尔硫dimeflin 回苏灵diphtheria 白喉diplegia 双侧瘫痪diploe 板障diplomyelia 脊髓纵裂diplopia 复视dipyridamole 潘生丁discobolus attitude 掷铁饼姿势(半规管受刺激) disequilibrium平衡不稳disorded action of the heart 神经性循环衰弱disorientation 定向障碍disseminated sclerosis 播散性硬化dissociated sensory loss 分离性感觉丧失distal muscular dystrophy 远端肌营养不良症disulphiram 戒酒硫disuse handicap 废用性缺陷dizziness 眩晕dlo-tocopherol nicatinate 烟酸生育酚酯dobutamine 多巴酚丁胺dogmatil 硫苯酰胺dominant hemisphere 优势半球dopaminergic pathway 中脑多巴胺能通路Dorsal disc prolapse 椎间盘突出症dorsal intermedian suleus 后中间沟dorsal longitudinal fasciculus 背侧纵束dorsal median suleus 后正中沟dorsal thalamus 背侧丘脑dorsal 背侧dorsiflexion 背屈Down syndrome 唐综合征Dowson encephalitis 亚急性包涵体脑炎doxepine 多虑平doxycycline 强力霉素dramamine 茶苯海明dribbling流涎drop seizure跌倒发作drowsy 瞌睡drunken gait 酒醉步态Duchenne muscular dystrophy 杜兴氏肌营养不良Duchenne-Erb paralysis 杜-欧麻痹dura mater 硬膜duxil 都可喜dwarfism 侏儒症dysantigraphia 抄写不能dysaphia 触觉障碍dysaptation 眼调节不良dysarthria 构音困难dysaudia 听力障碍dysautonomia 家族性自主神经机能异常dysbasia 步行障碍dyscalculia 计算困难dyschiasia 定位觉障碍dyschiria 左右感觉障碍dyschronism 定时障碍dyscoimesis 睡眠障碍dyscoria 瞳孔反应异常dysdiadochokinesia 轮替运动障碍dysequilibrium 平衡失调dysergasia 整体反应障碍dysergia 传出性共济失调dysesthesia 感觉障碍dysgrammatism 语法错乱dysgraphia 书写困难dyskinesias 动作障碍dyslalia 言语障碍dyslexia 诵读障碍dyslexic 阅读不能dysmnesia 记忆障碍dysmyotonia 肌张力障碍dysopia 视觉障碍dysosmia 嗅觉障碍医学全.在线提供dysphgia 吞咽障碍dysphonia 发音困难dysphrasia 言语困难dysphrenia 精神障碍dyspnoea 呼吸障碍dysponesis 皮层运动区活动障碍dyspraxia 运用障碍dysrhaphia 神经管闭合不全dysrhaphism 脊柱裂dysrythmia 节律障碍dysstasia 起立困难dyssynergia 肌协同失调dyssynergia 协同障碍dystaxia 共济失调dystects 神经管闭合不全dystonia musculorum deformans 变形性肌张力障碍dystonia 肌张力障碍dystrophia myotonica 肌营养不良性肌强直症dystrophy 肌营养不良EEaton-Lambert myasthenic syndrome 重症肌无力综合征echinococcus 绦虫病Echo virus 埃可病毒echoencephalogram 脑超声图echylnandrol 乙基雌烯醇Ecker's fissure 枕横沟ectethmoid 筛骨外侧部ectoglia 外神经胶质ectopia 异位ectorhinal area 嗅外区Edinger's law 埃丁格尔定律edrophonium 腾喜龙effector in viscers 内脏效应器effector, motor ending 效应器efferent 传出eicosapentaenoic acid, EPA 二十碳五烯酸Eimer's organ 埃米尔氏器Elanolz's bodies 埃尔兹霍兹体(有髓神经纤维变性小体) elastase 弹性酶electrical synapse 电突触electroconvulsive therapy 电惊厥疗法electrocorticography 脑皮层电图electroencephalography 脑电图electroencephaloscope 脑电镜electrolyte 电解质electromyography 肌电图electron microscope 电子显微镜electroneurography 神经电图electronystagmography 眼震电图electro-oculogram 眼电图electrophoresis 电泳electroplexy 电休克electroretinogram 视网膜电图electrospinogram 脊髓电图elicited 引出emboli 栓子ement 充血emepronine 乙基二甲二苯溴丙胺eminence 隆起empty sella syndrome 空蝶鞍综合征encephalitis lethargica 昏睡性脑炎encephalitis 脑炎encephalitogenic 致脑炎的Encephalitozoon rabiei 内格里小体(狂犬病包涵体) encephalization 脑形成encephalo-arteriography 脑动脉造影术encephalocele 颅腔encephaloclastic 脑损害的encephalocystocele 积水性脑突出encephalodialysis 脑软化encephalodysplasia 脑发育异常encephalogram 脑造影照片encephalography 脑照相术encephaloid 髓样瘤encephalolith 脑石encephaloma 脑瘤encephalomalacia脑软化encephalomeningitis 脑膜脑炎encephalomeningocele脑脑膜膨出encephalomeningopathy 脑脑膜病encephalomere 脑节encephalomyelitis 脑脊髓炎encephalomyeloneurophy 脑脊髓神经病encephalomyelopathy 脑脊髓病encephalomyeloradiculitis 脑脊髓神经根炎encephalomyeloradiculoneuritis 脑脊髓神经根神经炎encephalomyeloradiculopathy 脑脊髓脊神经根病encephalomyocarditis 脑心肌炎encephalonarcosis 脑病性木僵encephalopathy 脑病encephalopuncture 脑穿刺术encephalopyosis 脑脓肿encephaloradiculitis 脑脊神经根炎encephalorrhagia 脑出血encephalosclerosis 脑硬化encephaloscope 窥脑镜encephalosepsis 脑坏疽医.学全在.线提供encephalosis 器质性脑病。

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