Failure of dipyridamole (Persantin) in reducing the infarct size following experimental coronary occlusion.

Abstract

This study examined the systemic and coronary hemodynamic effects of dipyridamole on experimental myocardial infarcts. Electrograms were recorded from the left ventricular surface 15min. after ligation of the left anterior descending coronary artery. Average ST segment elevation and number of sites with ST segment elevation greater than 2mV., indices of the magnitude and extent of acute myocardial ischemic injury, were increased in 9 dogs following intravenous infusion of dipyridamole (0.01-0.05mg./Kg./mm.) from 4.6±0.3 (Mean value±SEM) during control simple occlusion to 6.8±0.9mV. (p<0.025), and 6.2±0.6 to 8.1±1.2 (p<0.05), respectively. This was accompanied by significant decreases in mean blood pressure from 105±5 to 79±6mm.Hg (p<0.025) and in mean value of coronary perfusion pressure index (Mean blood pressure×Heart rate×Diastolic duration in aortic pressure) from 4, 100±180 to 3, 130±210mm.Hg sec./min. (p<0.01), respectively. Coronary blood flow measured by a flow probe applied around the root of the circumflex coronary artery was markedly increased from the mean value of 115±6 during control occlusion to 284±45 (arbitrary unit, p<0.01).Thus, we concluded that dipyridamole does have deleteriou effects on acute myocardial ischemic injury by reducing coronary perfusion pressure which importantly influence the blood supply to the ischemic zone of myocardium, in spite of augmented total coronary blood flow.