中南大学生理学06-减压神经放电与动脉血压调节

减压神经放电与动脉血压的调节
Depressor nerve discharge and the regulation of arteriole blood pressure 【教学对象与学时】
一、教学对象：五年制本科
二、学时：4学时
【预习要求】
理论：减压反射过程，动脉血压调节的方式
操作：家兔减压神经走行，颈总动脉的解剖，前后的相邻关系，
【目的要求】
操作: 家兔颈总动脉、颈迷走神经和内脏大神经的解剖位置及其分离，减压神经放电的引导，颈动脉插管法
理论: 心血管的神经支配动脉, 血压相对恒定的机制及生理意义，减压反射在其中的作用
【重点和难点】
重点：动脉插管，插管凝血；减压神经的辨认，分离和放电的引导。

难点：内脏大神经的分离
【教学过程设计】
1.课前提问和预习检查
2.讲解血压的调节及影响因素
3.介绍家兔颈总动脉、颈迷走神经和内脏大神经的解剖位置及其分离，减压神经放电
的引导，颈动脉插管法。

4.实验结束前汇总全班实验结果，讨论比较体位和不同运动强度对血压和心率的影
响，理解在不同生理情况下心血管的整合反应。

【课前预习检查或提问】
一、什么是动脉血压？
二、影响动脉血压的因素有哪些？
三、减压神经属什么神经？参与何种反射？
【课前讲解】
一、设计原理直接插管于颈总动脉，将动脉血压的变化经压力换能器转变为电信号，
由生物信号记录系统记录，兔主动脉弓压力感受器的传入神经在颈部自成一束，即减压神经，故可较方便地引导其放电。

减压神经放电随动脉血压波动而变化。

用牵拉和夹闭颈总动脉分别模拟动脉血压升高和降低对颈动脉窦的刺激作用，借以观察减压反射及其在动脉血压调节中的作用。

二、基本操作技术和仪器参数
1、动物的麻醉与固定见实验指导
2、分离减压神经于颈正中作一长约7cm的切口，分离皮下组织及肌肉，暴露颈总动
脉以及与之并行的神经。

仔细辨认三条神经，迷走神经最细，规整，明亮，交感神经较细较暗，减压神经最细。

迷走神经位于最外侧，减压神经往往位于迷走神经和交感神经之间。

用玻璃分针小心分离减压神经2－3cm，穿线备用。

3、分离颈总动脉及动脉插管见实验指导
4、分离左侧内脏大神经
三、观察项目
1、正常情况下减压神经放电和血压
2、加乙酰胆碱
3、加去甲肾上腺素
4、牵拉左颈总动脉
5、夹闭右颈总动脉
6、剪断右迷走神经，刺激其外周端；
7、注射Adr
8、分离刺激内脏大神经分别从减压神经中枢端和外周端进行引导。

四、注意事项
1、及时止血，保持手术野清楚
2、分离动脉、神经时，切勿用手术刀或有齿镊
3、对减压神经辨认清楚后再分离，切勿损伤，并常滴加石蜡油，以防干燥。

4、动脉插管粗细要适宜，管口不宜过尖
5、动脉插管应尽量靠动脉头端进行，结扎要可靠，但不要用力过大。

保留远心端结扎
线，备牵拉用。

6、切勿使血液流入换能器，如有此现象，需关闭三通管，及时处理。

7、如插管处出现凝血现象，可根据不同情况，分别处理，如注入一些肝素，回抽血块
或重新插管。

【典型结果】
项目减压神经放电动脉血压
频率幅度基线频率幅度基线
【分析讨论】（略）
【参考结论】（略）
【实验报告要点】
一、正确剪贴和标注原始记录，无记录者可临摹原始记录或绘表格填写结果
二、描绘血压与减压神经放电的波形，分析二者的关系
三、简要解释所观察到的实验结果，并归纳出相应结论。

【思考题及参考答案】
一、减压反射弧的构成
二、如在靠近颈动脉窦的上方阻断血流，对血压有何影响？
三、为什么要切断迷走神经，再刺激外周端？
四、如何进一步证明减压神经对血压的调节作用？
【参考内容】
【专业英语选读】
Integrative Cardiovascular Physiology
Reflex control of the circulation. Overall regulation of the cardiovascular system requires neurogenic and endocrine mechanisms superimposed on intrinsic controllers of the heart and blood vessels.In 1866, deCyon and Ludwig (33) showed that stimulation of the aortic depressor nerve caused a reflex bradycardia and arterial hypotension, providing testimony to the ability of afferent nerves to influence the behavior of the cardiovascular system. In 1903,Köster and von Tschermak (92) found that the frequency of action potentials measured in the depressor nerve increased with distension of the aorta. The carotid baroreceptors were discovered in 1923by Hering (73). Subsequently, Bronk and Stella (18) established the proportional relationship between carotid sinus baroreceptor firing rate and distension of the vessel wall. The ability of the baroreceptors to adapt was demonstrated by Heymans (75) in 1950, using vasoactive agents applied to the baroreceptive surface. In 1957, McCubbin et al. (109) found resetting of the baroreceptors in chronic arterial hypertension, suggesting adaptation to chronic distension.
The concept of mechanoreceptor reflexes initiated in the atria was introduced by Bainbridge (7) in 1915. In 1956, Henry,Gauer, and Reeves (72) provided evidence for the atrial location of receptors influencing urine flow, suggesting a reflex mechanism for regulation of blood volume. The following year, Baisset and Montastruc (6) demonstrated that the renal effect was due to a reflex reduction in circulating levels of antidiuretic hormone.A more direct link between atrial distension and cardiovascular functions involving release of natriuretic proteins from granules stored in atrial myocytes was uncovered by DeBold (32) in1981.
In 1933, Heymans (74) discovered the chemoreceptor reflex and the ability of receptors located in the carotid sinus and aortic arch to monitor the chemical composition of arterial blood.A reflex arterial hypertension and cardioacceleration arising from nerve endings in skeletal muscle of humans were demonstrated by Alam and Smirk (1) in 1937. Mitchell (113) revisited this issue in 1977 and subsequently demonstrated the ability of muscle afferents to respond to the metabolites released from contracting muscle.
Claude Bernard (12) presented evidence for the existence of vasomotor nerves in 1851. Two years later, Schiff (154) sectioned the brain stem and spinal cord to show that neurogenic vasomotor activity originated from higher centers of the central nervous system. In 1908, Bayliss (see Ref.
9) proposed the existence of a vasomotor center that orchestrated vasoconstrictor and vasodilatory influences through efferent nerves. In
the middle of this century,Shipley and Gregg (159) and Randall and colleagues (138) delineated the efferent pathways projecting to the heart. In 1946, Alexander(2) stressed the tonic and reflex functions of the medullary cardiovascular center. More recently, the loci of cardiovascular integration in the central nervous system have been extended from the medulla upward to hypothalamic, limbic, and other forebrain regions, as well as downward to the spinal cord (91).
Hormonal control of the circulation. The existence of a vasoconstrictor system dependent on the kidney was suggested by the studies of Goldblatt (60), who showed that impairment of renal perfusion led to arterial hypertension. In 1898, Tigerstedt and Bergman (173) discovered renin. Forty years later Braun-Menendez(17) and Page (125) independently identified angiotensin as the product of renin action.
Overall regulation of the circulation. The interactions of the heart and blood vessels required to achieve cardiovascular homeostasis are complex and difficult to conceive and explore without the help of conceptual and mathematical models. In 1955,Guyton (62a) developed a graphical analysis based on simultaneous plots of cardiac function and venous return curves. The point of intersection of the two graphs represented the steady-state level of cardiac output on the y-axis and the mean atrial filling pressure on the x-axis. The impact of neurogenic and hormonal influences on each of the cardiac function and venous return curves allowed the determination of the overall impact of the specific disturbances on cardiovascular behavior. In 1967, Guyton and Coleman(64) proposed a model to integrate the interactions of the heart,blood vessels, and kidney in the long-term regulation of arterial blood pressure. The concept emphasized the role of the kidney as the primary determinant of the arterial pressure over the long term. Later, intrinsic and extrinsic regulation of blood flow
in different vascular beds, baroreceptor and chemoreceptor reflexes,and hormonal influences were added to the basic renal-body fluid loop to help predict cardiovascular responses to different perturbations(65).
参考文献
1、姚泰主编，人体生理学，第三版，北京：人民卫生出版社，2001
2、姚泰，罗自强主编. 生理学（七年制规划教材），北京：人民卫生出版社，2001。