Coronary vascular effects of cocaine in rats.

It has been suggested that ischemia secondary to coronary vasoconstriction is responsible for adverse cardiovascular effects of cocaine. However, the reported coronary vascular effects of cocaine vary considerably. We sought to determine the effects of cocaine on the coronary vasculature in anesthetized and conscious rats. Rats anesthetized with chloralose were instrumented for estimation of ascending aortic and coronary blood flows using pulsed Doppler velocitometry. Cocaine administration resulted in bradycardia and a biphasic mean arterial pressure response. Cocaine elicited highly variable increases in coronary vascular resistance and decreases in cardiac output. Decreases in coronary blood flow and rate-pressure product were directly correlated. Prazosin significantly attenuated the cardiac output but not the coronary vascular responses to cocaine. Propranolol, on the other hand, significantly shortened the duration of both responses. Conscious rats, instrumented for coronary blood flow determination, also exhibited cocaine-induced increases in coronary vascular resistance, yet the changes in coronary blood flow were not correlated with the rate-pressure product. These results provide the first evidence that cocaine produces equivalent increases in coronary vascular resistance in conscious and anesthetized rats. However, because the relationship between coronary blood flow and rate-pressure is different between the two preparations, as are other cardiovascular responses, we suggest that anesthesia alters the mechanism(s) by which cocaine affects the rat coronary vasculature.