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犬实验性心肌缺血中心脏交感神经驱动的减弱

Attenuation of cardiac sympathetic drive in experimental myocardial ischemia in dogs.

作者信息

Feola M, Arbel E R, Glick G, Ellis A

出版信息

Am Heart J. 1977 Jan;93(1):82-8. doi: 10.1016/s0002-8703(77)80175-0.

Abstract

Sympathetic discharges to the heart were recorded from the left inferior cardiac nerve of 16 dogs. Inferior cardiac nerve activity (ICNA) under normal conditions consisted of grouped discharges, synchronous with the cardiac cycle and modulated by respiration. After ligation of the circumflex branch of the left coronary artery, ICNA declined concomitant with a decline in heart rate and mean aortic pressure. After 30 minutes, when arterial pressure tended to recover toward control values (six dogs), ICNA remained low; in contrast, when arterial pressure dropped to shock levels (three dogs), ICNA increaed. When aortic pressure fell precipitously as a result of ventricular fibrillation, even during the first 30 minutes of ischemia (seven dogs), ICNA immediately increased greatly. The results of this study suggest that acute coronary occlusion produces a cardiocardiac depressor reflex with attenuation of sympathetic discharge to the heart. This reflex, under the experimental conditions studied, gives way to the baroreceptor reflex when aortic pressure drops to critically low levels.

摘要

从16只狗的左下心脏神经记录了心脏的交感神经放电。正常情况下,心脏下神经活动(ICNA)由成组放电组成,与心动周期同步并受呼吸调节。结扎左冠状动脉回旋支后,ICNA下降,同时心率和平均主动脉压也下降。30分钟后,当动脉压趋于恢复到对照值时(6只狗),ICNA仍保持较低水平;相反,当动脉压降至休克水平时(3只狗),ICNA增加。当由于心室颤动导致主动脉压急剧下降时,即使在缺血的最初30分钟内(7只狗),ICNA也会立即大幅增加。本研究结果表明,急性冠状动脉闭塞会产生心脏抑制反射,导致心脏交感神经放电减弱。在本研究的实验条件下,当主动脉压降至极低水平时,这种反射会让位于压力感受器反射。

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