Complications of cocaine administration are acute vascular occlusions such as myocardial infarction and stroke. We have studied the influence of cocaine on platelet function in vitro. For that purpose, citrated blood from healthy volunteers was incubated with cocaine concentrations of 0 (control), 10, 100, 1000, 2500, and 10'000 μmol/l plasma. Platelet aggregation was measured in whole blood under high shear flow conditions with a platelet function analyzer PFA-100 using either epinephrine (EPI) or ADP as a platelet activator, as well as in non-flowing blood measuring the change of impedance after the addition of either collagen or ADP (Chronolog-700 Aggregometer). In addition, platelet aggregation was measured by the change in light transmission in platelet rich plasma containing the same cocaine concentrations (Chronolog-700). Platelet aggregation in flowing whole blood (PFA-100) was not affected by cocaine up to 1000 μmol/l, partially inhibited by 2500 μmol/l and completely inhibited by 10'000 μmol/l cocaine. In non-flowing blood, platelet aggregation was decreased already at cocaine concentrations of 1000 μmol/l with ADP and 2500 μmol/l with collagen as a platelet activator. In platelet-rich plasma, aggregation was partially inhibited by 1000 and 2500 μmol/l and completely inhibited by 10'000 μmol/l cocaine. We conclude that platelet aggregation is inhibited by cocaine in vitro. This occurs, however, at concentrations above those measurable in vivo. These observations make it very unlikely that a direct platelet activation plays a role in vascular events complicating cocaine consumption.
Keywords: Cocaine; platelet aggregation.