Prostaglandin-induced preservation of the ischemic myocardium.

Abstract

SUMMARY The effectiveness of prostaglandin (PG) E,, E2, and F2a in altering responses to acute myocardial ischemia was studied in anesthetized, open-chest cats. Following coronary artery occlusion to induce myocardial ischemia (MI) or sham operation (sham MI), a PG (or its appropriate vehicle) was infused at 1 /*g/kg per minute for the 5-hour experimental period. Arterial blood pressure dropped significantly during PG infusion, whereas heart rate decreased only slightly. A pressure-rate index was significantly reduced in ischemic cats infused with either PGE, or PGE2. These two groups also failed to show large elevations in S-T segment which were usually observed in ischemic cats receiving PGF2a or 0.9% NaCI. Arterial blood samples (i.e., at 5 hours) showed significantly increased plasma creatine phosphokinase (CPK) specific activities in MI cats receiving PGF2a or NaCI, whereas PGE, and PGE, infusions prevented significant elevations in plasma CPK during ischemia. Myocardial tissue samples from ischemic cats receiving either PGF2a or NaCI showed significantly reduced tissue CPK in ischemic myocardial tissue. However, PGE, or PGE2 prevented decreases in myocardial CPK activity. Infusion of either Etype PG was further shown to prevent labilization of myocardial lysosomes in ischemic tissue, without significantly altering free amino-nitrogen concentrations in ischemic tissue. Thus, infusion of E-type prostaglandins significantly improved the hemodynamic status and moderated the leakage of enzymes from ischemic myocardial tissue in the cat. These prostaglandins may protect ischemic myocardial tissue by reducing cardiac oxygen demand and stabilizing cardiac lysosomal membranes.