Platelet Depletion and Infarct Size in an Occlusion Reperfusion Model of Myocardial Ischemia in Anesthetized Dogs

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Abstract
The formation of platelet aggregates and release of platelet-derived vasoactive mediators were suggested to aggravate ischemic myocardium. The contribution of platelets to myocardial damage induced by 90 min occlusion and 5 h reperfusion in chloralose-anesthetized dogs was assessed after depletion of platelets with specific antidog platelet antiserum. Dogs treated with antiplatelet antiserum showed > 90% reduction in circulating platelets and serum TxB2 [thromboxane B2] levels, but showed no reduction in infarct size (58 .+-. 3 vs. 51 .+-. 3% of risk area for control and thrombocytopenic dogs, respectively). Platelet depletion had no hemodynamic effect during the occlusion or reperfusion phases, nor reduced the incidence of arrhythmias. Platelet aggregates or platelet-derived mediators do not contribute directly to the extent of damage in this occlusion-reperfusion model of myocardial ischemia.