Objectives: Cardiovascular complications of cocaine use represent an important clinical problem, yet the mechanisms by which cocaine predisposes to myocardial ischemia are poorly understood.
Background: The effects of cocaine on the coronary circulation have been studied extensively in experimental animal models, but have failed to recapitulate the clinical findings reported in humans who use cocaine.
Methods: We studied 12 conscious, chronically instrumented dogs and 5 conscious, chronically instrumented baboons to determine whether there were important species differences in the response to cocaine.
Results: Comparable doses of intravenous cocaine caused similar increases in left ventricular systolic, diastolic and mean arterial pressure in the two species. However, the peak coronary blood flow response in baboons (+8 +/- 3 from 47 +/- 6 ml/min) was less compared with dogs (+15 +/- 4 from 41 +/- 4 ml/min), while the coronary vascular resistance response was greater in baboons (+0.60 +/- 0.09 from 1.94 +/- 0.09 mm Hg/ml/mm) compared with dogs (+0.35 +/- 0.09 from 2.24 +/- 0.10 mm Hg/ml/min). Although myocardial oxygen consumption responses were similar between species, there was a significant difference (p < 0.05) in oxygen delivery between baboons (+164 +/- 47 from 705 +/- 59 ml of oxygen per minute) and dogs (+397 +/-51 from 656 +/- 33 ml of oxygen per minute) that was attributable to a significant (p < 0.05) increase in hemoglobin concentration in dogs (+2.1 +/- 0.5 g/dl) that was not observed in baboons. Consequently, cocaine caused a significant increase in myocardial oxygen extraction and decreased coronary sinus pH in baboons, but not dogs.
Conclusions: Cocaine caused greater coronary vasoconstriction and greater requirements for oxygen extraction in baboons compared with dogs.