Urgent coronary revascularization for acute myocardial ischemia results in an increased mortality and morbidity. Deposition of activated platelets and leukocytes into the ischemic myocardium during reperfusion may augment perioperative ischemic injury. Dipyridamole reduces platelet activation and may reduce myocardial deposition and prevent ischemic injury during reperfusion. The effects of dipyridamole on myocardial platelet and leukocyte deposition were evaluated in a canine model of acute regional myocardial ischemia with reperfusion during cardioplegia on cardiopulmonary bypass. Eight dogs underwent left anterior descending (LAD) coronary artery ligation for 45 min followed by cardiopulmonary bypass and release of the ligature during 60 min of cold crystalloid cardioplegic arrest to stimulate urgent revascularization. Four dogs were randomized to receive an infusion of dipyridamole perioperatively (50 mg/hr) and 4 dogs served as controls. Autologous platelets were labeled with 111In, leukocytes with 99mTc, and erythrocytes with 51Cr. The labeled cells were infused immediately after cross-clamp release and myocardial biopsies were obtained at 10, 20, 30, and 60 min of reperfusion. Platelets were deposited in the myocardium during reperfusion and four times more platelets were found in the LAD region than the circumflex region. Leukocyte deposition was similar in the LAD and circumflex regions. Dipyridamole reduced both platelet and leukocyte deposition and the reduction was greater in the LAD than in the circumflex region. Myocardial platelet and leukocyte deposition was found after regional ischemia, cardioplegia, and cardiopulmonary bypass. Dipyridamole reduced myocardial platelet and leukocyte deposition and may reduce perioperative ischemic injury.
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