EARLY PROSTAGLANDIN RELEASE FROM ISCHEMIC MYOCARDIUM IN DOG

Abstract

Cellular consequences of myocardial ischemia were studied in anesthetized dogs. Confirmation of myocardial ischemia was provided by ECG and biochemical indexes. Prostaglandin F2.alpha. release into coronary venous blood was significantly elevated during myocardial ischemia, whereas indomethacin treatment prevented this increase in coronary venous prostaglandin F2.alpha. concentrations. No significant increase in prostaglandin E2 release was observed in response to myocardial ischemia, but indomethacin treatment significantly reduced coronary venous prostaglandin E2 concentrations below those of control values. Within 1 h after occlusion of the coronary artery, the S-T segment was significantly altered, and coronary venous prostaglandin F2.alpha. increased significantly above the control concentration. These changes persisted during 4 h of myocardial ischemia. Plasma creatine phosphokinase activity increased significantly after 2 h of myocardial ischemia and remained elevated for the subsequent 2 h of ischemia. After 4 h of myocardial ischemia, myocardial creatine phosphokinase activity of ischemic myocardium was significantly reduced, and labilization of myocardial lysosomes occurred in ischemic tissue. Indomethacin treatment prevented increases in prostaglandin release but did not influence other biochemical changes or the ECG response to ischemia. Prostaglandin release by ischemic myocardial tissue is an early response to the ischemic stimulus.