Cardiac function during vagus escape.
It is generally believed that the stimulation of vagus nerve has no direct effect on ventricular myocardium. But recent work has demonstrated clear-cut negative inotropic effect of vagal stimulation on ventricles. In an attempt to study further the effect of vagal stimulation on heart, 15 dogs were studied hemodynamically under nembutal anaesthesia. Bilateral vagotomy caused 9% elevation of heart rate whereas arterial pressure and cardiac output increased by 5% and 3% respectively. Stroke volume output decreased by 8%. Stimulation of the cut peripheral end of vagus caused cardiac standstill followed by vagus escape. During the steady state of vagus escape there was marked reduction in arterial pressure, heart rate and cardiac output, but the stroke volume was significantly elevated above the mean control. These findings suggest that when heart rate decreases, the stroke volume increases in order to restore the decreased cardiac output and that this happens inspite of the negative inotropic effect of vagal stimulation. Thus the Frank-Starling mechanism has a very significant role in an intact organism with normal hemodynamics.
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D006321:Heart / Q000294:innervation / Q000502:physiology*; D006339:Heart Rate; D008297:Male; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*