Reflex control of ventricular refractoriness in the nonischemic myocardium during coronary occlusion.
The purpose of the study was to determine whether activation of cardiac receptors and arterial baroreceptors by myocardial ischemia could elicit reflex alteration of the effective refractory period (ERP) of nonischemic ventricular myocardium in cats. Changes in ERP of nonischemic area of the right ventricle and mean arterial pressure (MAP) were measured during transient left anterior descending (LAD) coronary artery occlusion in anesthetized cats. LAD coronary occlusion for 90 sec caused a small but significant shortening of ERP (maximal change = 2.5 +/- 2.3 msec) associated with a decrease in MAP. Vagotomy significantly augmented the shortening of ERP to -3.4 +/- 1.6 msec and attenuated the decrease in MAP. After selective cardiac sympathectomy, the reflex response in refractoriness was virtually abolished. In cats with sinoaortic denervation with intact sympathetic nerves, marked attenuation was observed in the reflex change in refractoriness, although the decrease in MAP was significantly greater. These results indicate that: (1) autonomic reflexes activated during acute myocardial ischemia shorten the refractory period of nonischemic ventricular myocardium; (2) the reflex response is predominantly mediated by enhancement of cardiac sympathetic nerve activity resulting from the reduced baroreceptor activity due to concurrent hypotension.
D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D002415:Cats; D003327:Coronary Disease / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D009200:Myocardial Contraction; D009431:Neural Conduction; D011311:Pressoreceptors / Q000503:physiopathology; D012018:Reflex; D012032:Refractory Period, Electrophysiological; D013562:Sympathectomy; D014628:Vagotomy; D014630:Vagus Nerve / Q000503:physiopathology