Cerati D, Schwartz P J
Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Italy.
Circ Res. 1991 Nov;69(5):1389-401. doi: 10.1161/01.res.69.5.1389.
Experimental and clinical evidence indicates that high risk for sudden death is significantly correlated with post-myocardial infarction depression in two "markers" of vagal activity, heart rate variability and baroreflex sensitivity. The present experiments were designed to answer some of the questions generated by those findings. In 33 anesthetized cats, the neural activity of single cardiac vagal efferent fibers was recorded in control conditions and after injection of phenylephrine (n = 33), before and during a 1-hour coronary artery occlusion (CAO) (n = 17), and before and after removal of the left stellate ganglion (n = 16). In the first minute after CAO, vagal activity increased by 35% from 1.66 +/- 0.37 to 2.57 +/- 0.62 impulses/sec (p less than 0.01); despite a slight decline, it remained for the entire CAO above the control values, to which it returned after CAO release. Of 17 cats, ventricular fibrillation occurred in nine (susceptible) and eight survived (resistant). Resistant and susceptible cats had different reflex vagal responses to CAO. Whereas the resistant cats had a 48% (p less than 0.01) increase by the second minute of CAO, susceptible cats had no change (-18%, p = NS) in vagal activity. These differences were independent of blood pressure changes. The increase in vagal efferent activity in response to the blood pressure rise induced by phenylephrine (baroreceptive reflex) was more marked in the resistant cats compared with the susceptible cats (+246 +/- 66% versus +80 +/- 14%, p less than 0.025). Just before the injection of phenylephrine, vagal activity was not different between resistant and susceptible cats (1.58 +/- 0.35 versus 1.48 +/- 0.30 impulses/sec, p = NS). In 16 cats, left stellectomy increased cardiac vagal efferent activity by 75% (p less than 0.01), and the reflex vagal activation secondary to phenylephrine was further enhanced (from 2.2 +/- 0.4 to 4.7 +/- 0.7 impulses/sec, p less than 0.001). These data demonstrate that 1) cardiac vagal efferent activity increases in response to acute myocardial ischemia--much more so among the animals destined to survive, 2) before CAO, susceptible and resistant animals can be identified by the vagal response to blood pressure increase (assessed clinically by baroreflex sensitivity) and not by tonic vagal activity (assessed clinically by heart rate variability), and 3) the findings with left stellectomy support the hypothesis that vagal activity decreases after myocardial infarction because of an increase, secondary to abnormal stretch of the cardiac mechanoreceptors, in cardiac sympathetic afferent traffic, which exerts a tonic restraint on vagal outflow.
实验和临床证据表明，在迷走神经活动的两个“标志物”——心率变异性和压力反射敏感性方面，猝死的高风险与心肌梗死后抑郁症显著相关。本实验旨在回答这些发现所引发的一些问题。在33只麻醉猫中，记录了单个心脏迷走神经传出纤维在对照条件下、注射去氧肾上腺素后（n = 33）、1小时冠状动脉闭塞（CAO）前和期间（n = 17）以及切除左侧星状神经节后和切除后（n = 16）的神经活动。在CAO后的第一分钟，迷走神经活动从1.66±0.37增加到2.57±0.62次/秒，增加了35%（p<0.01）；尽管略有下降，但在整个CAO期间仍高于对照值，并在CAO解除后恢复到对照值。在17只猫中，9只（易感）发生心室颤动，8只存活（抗感）。抗感和易感猫对CAO的反射性迷走神经反应不同。抗感猫在CAO的第二分钟时迷走神经活动增加了48%（p<0.01），而易感猫的迷走神经活动没有变化（-18%，p =无显著性差异）。这些差异与血压变化无关。与易感猫相比，抗感猫对去氧肾上腺素引起的血压升高（压力感受性反射）的迷走神经传出活动增加更为明显（分别为+246±66%和+80±14%，p<0.025）。在注射去氧肾上腺素之前，抗感和易感猫的迷走神经活动没有差异（分别为1.58±0.35和1.48±0.30次/秒，p =无显著性差异）。在16只猫中，左侧星状神经节切除术使心脏迷走神经传出活动增加了75%（p<0.01），而去氧肾上腺素继发的反射性迷走神经激活进一步增强（从2.2±0.4增加到4.7±0.7次/秒，p<0.001）。这些数据表明：1）急性心肌缺血时心脏迷走神经传出活动增加——在注定存活的动物中增加得更多；2）在CAO之前，易感和抗感动物可以通过对血压升高的迷走神经反应（临床上通过压力反射敏感性评估）而不是通过紧张性迷走神经活动（临床上通过心率变异性评估）来识别；3）左侧星状神经节切除术的结果支持这样的假设，即心肌梗死后迷走神经活动降低是由于心脏机械感受器异常伸展继发心脏交感神经传入流量增加，从而对迷走神经传出产生紧张性抑制。
