Minisi A J, Cersley T L
Department of Medicine, Medical College of Virginia/Virginia Commonwealth University, Richmond.
Circulation. 1994 Oct;90(4):2015-21. doi: 10.1161/01.cir.90.4.2015.
Cardiac transplantation and chronic myocardial infarction interrupt vagal afferent nerve fibers, which originate mainly from the ventricles. Marked abnormalities of reflexes mediated by cardiopulmonary receptors with vagal afferent fibers have been demonstrated after both cardiac transplantation and chronic myocardial infarction. The relation between these reflex abnormalities and ventricular deafferentation is not known.
To further assess this relation, we investigated the effects of left ventricular (LV) deafferentation on the control of renal sympathetic nerve activity (RSNA) by the vagal cardiopulmonary reflex in chloralose-anesthetized, mechanically ventilated dogs with sinoaortic denervation. Responses of left atrial pressure (LAP) and RSNA to hemorrhage and volume expansion were measured before and after application of 88% phenol to either the inferoposterior LV (n = 12) or the entire LV (n = 14). In control experiments, measurements were made before and after application of saline to the LV (n = 12). Reflex sensitivity (percent change in RSNA per mm Hg change in LAP) measured during volume expansion was mildly attenuated after both total (prephenol, -9.1 +/- 0.7; postphenol, -6.6 +/- 0.7; P < .05) and inferoposterior (pre, -12.5 +/- 1.8; post, -8.1 +/- 0.6; P = .055) LV deafferentation. Reflex sensitivity measured during hemorrhage was not significantly altered by inferoposterior or total LV deafferentation. Epicardial saline had no significant effect on reflex sensitivity values measured during either volume expansion or hemorrhage. Reflex inhibition of RSNA in response to intracoronary nicotine was abolished after phenol application, indicating adequate ventricular deafferentation. Phenol application had no significant effect on LAP-myocardial segment length relations measured by sonomicrometry (n = 6).
Interruption of vagal afferent input from the LV has only modest effects on the control of RSNA by the vagal cardiopulmonary reflex. These data indicate that there is considerable redundancy in the vagal cardiopulmonary reflex such that receptors from the lungs and other cardiac chambers can largely compensate for the loss of afferent input from the LV.
心脏移植和慢性心肌梗死会中断主要起源于心室的迷走传入神经纤维。心脏移植和慢性心肌梗死后，由具有迷走传入纤维的心肺感受器介导的反射出现了明显异常。这些反射异常与心室去传入神经之间的关系尚不清楚。
为了进一步评估这种关系，我们在氯醛糖麻醉、机械通气且去窦弓神经的犬中，研究了左心室（LV）去传入神经对迷走心肺反射控制肾交感神经活动（RSNA）的影响。在向左心室下后壁（n = 12）或整个左心室（n = 14）应用88%苯酚前后，测量左心房压力（LAP）和RSNA对出血和容量扩张的反应。在对照实验中，在向左心室应用生理盐水前后进行测量（n = 12）。在容量扩张期间测量的反射敏感性（LAP每变化1 mmHg时RSNA的变化百分比）在整个左心室（应用苯酚前，-9.1±0.7；应用苯酚后，-6.6±0.7；P <.05）和下后壁左心室去传入神经后（应用前，-12.5±1.8；应用后，-8.1±0.6；P = 0.055）均轻度减弱。在下后壁或整个左心室去传入神经后，出血期间测量的反射敏感性没有显著改变。心外膜生理盐水对容量扩张或出血期间测量的反射敏感性值没有显著影响。应用苯酚后，对冠状动脉内注射尼古丁引起的RSNA反射抑制作用消失，表明心室去传入神经充分。应用苯酚对通过超声心动图测量的LAP-心肌节段长度关系没有显著影响（n = 6）。
左心室迷走传入神经输入的中断对迷走心肺反射控制RSNA的影响较小。这些数据表明，迷走心肺反射存在相当大的冗余，使得来自肺和其他心腔的感受器能够在很大程度上补偿左心室传入神经输入的丧失。
