Abstract

Experiments were designed to compare the effects of cocaine on cardiac output, blood pressure, and total peripheral resistance responses to norepinephrine, tyramine, angiotensin, and stimulation of cardiac sympathetic nerves. The results indicate that in intact dogs the augmented pressor response to norepinephrine is primarily the result of a greater vascular effect of norepinephrine; it is not caused by a greater cardiac output. The pressor response to tyramine was decreased by cocaine primarily as the result of a decrease in its vascular effect rather than its effect on cardiac output. In these intact animals baroreceptor reflexes played the major role in regulating cardiac output responses to norepinephrine and tyramine. On the other hand, in dogs in which bilateral cervical vagotomy and the administration of atropine prevented reflex bradycardia, the pressor responses were caused predominantly by changes in cardiac output. In tese animals cocaine markedly augmented cardiac output responses to norepinephrine and slightly reduced cardiac output responses to tyramine. The results suggest that cocaine sensitized the inotropic more than the vascular effects of norepinephrine and that an inotropic effect of tyramine persisted when its vascular effect was antagonized. The cardiovascular responses to angiotensin, which served as an internal control, were unchanged by cocaine. The effect of cardiac sympathetic nerve stimulation on stroke work increased after cocaine, suggesting an increased inotropic effect.