A comparison was made of the effects of vasopressin (ADH), methoxamine (MX), and angiotensin II (AN) on coronary and left ventricular dynamics, cardiac output, and regional blood flow distribution in intact, consci9us dogs. At an equal percent pressure elevation, ADH reduced cardiac output and cardiac rate the most, while AN had the least effect. After denervation of arterial baroreceptors, ADH still reduced heart rate, while AN increased it, suggesting nonbaroreceptor negative and positive chronotropic effects, respectively. A differential pattern on peak dP/dt was also observed, with ACH causing a greater reduction than MX while AN did not decrease dP/dt. With heart rate held constant, AN did not reduce dP/dt, suggesting a direct positive inotropic effect since dP/dt should have fallen slightly due to reflex mechanisms, as was observed with MX and ADH. ADH induced the greatest increase in coronary resistance (140%), while the least (46%) was observed with AN, which could be explained, in part, by the differential effects observed on cardiac rate and contractility. The greatest increase in resistance in the iliac bed occurred with ADH (30%), and the least with AN (34%). Conversely, the greatest constriction in the renal bed occurred with AN (95%), and lesser amounts were observed with ADH (36%) and MX (35%). Thus ADH, MX, and AN exert potent yet differential vasoconstricting actions on peripheral beds. In addition, while all three agents elicited coronary vasoconstriction, the differential effects on coronary vascular resistance appeared to be due predominantly to a difference in chronotropic and inotropic actions.

Effects of anesthesia and sleep on circulatory response to carotid sinus nerve stimulation.

The purpose of the present investigation was to examine coronary flow and vasodilator reserve in conscious, chronically instrumented dogs with pacing-induced heart failure, a model of severe biventricular cardiomyopathy devoid of significant hypertrophy. Twelve dogs were studied after 28 days of rapid right ventricular pacing and were compared with six sham-operated controls. Left ventricular (LV) average transmural flow was significantly less in conscious dogs with pacing-induced heart failure, whereas the endocardial-to-epicardial flow ratio was not significantly different. In response to near maximal coronary vasodilation with adenosine, subepicardial coronary flow and vasodilator reserve were preserved in congestive heart failure (CHF), yet there was evidence of impaired subendocardial flow and vasodilator reserve, and the endocardial-to-epicardial ratio was significantly less. When the markedly elevated LV end-diastolic pressure was normalized in heart failure, there was restoration of subendocardial coronary flow reserve and a normalization of the endocardial-to-epicardial ratio. Thus, in CHF, there is impaired coronary flow and vasodilator reserve that is selective to the subendocardium of the LV. At this point in the heart failure process, this impairment is not associated with structural changes but is a consequence of the marked elevation in LV end-diastolic pressure.

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SUMMARY. We studied the effects of slow continuous hemorrhage (0.5 ml/kg per min) on measurements of arterial and left atrial pressures, and renal nerve activity in conscious dogs with all reflexes intact, or after sinoaortic baroreceptor denervation, cardiac denervation, or sinoaortic baroreceptor denervation plus vagal denervation. In intact dogs, mean arterial pressure remained relatively constant at 101 ± 4 mm Hg until 20 ± 4 ml/kg of hemorrhage, when renal nerve activity increased by 211 ± 53%. At 39 ± 2 ml/kg hemorrhage, mean arterial pressure fell by 48 ± 3 mm Hg, and renal nerve activity returned to the prehemorrhage control level. Cardiac denervation did not affect the response of mean arterial pressure to hemorrhage, whereas, after sinoaortic baroreceptor denervation and sinoaortic baroreceptor plus vagal denervation, mean arterial pressure remained at its control level only through 8 ± 1 and 4 ± 1 ml/kg hemorrhage, respectively. The increases in renal nerve activity during nonhypotensive hemorrhage were significantly attenuated by eitheT sinoaron'c baroreceptor or cardiac denervation, and were completely blocked by sinoaortic baroreceptor plus vagal denervation. However, the decline in renal nerve activity, with hypotensive hemorrhage was not blocked by either cardiac or sinoaortic baroreceptor denervation, and was enhanced after sinoaortic baroreceptor plus vagal denervation. Our data indicate that nonhypotensive hemorrhage in the conscious dog elicits a striking increase in renal nerve activity, which then returns to control levels during hypotensive hemorrhage. Both sinoaortic and cardiopulmonary baroreceptors are involved in mediating the increase in renal nerve activity, whereas the decline in renal nerve activity is not due to either of these baroreflexes. {CircRes 57: 788-793, 1985)