Prostaglandin-induced preservation of the ischemic myocardium.

Abstract

The effectiveness of prostaglandin (PG) E1, E2 and F2.alpha. 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 .mu.g/kg per min for the 5 h 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 PGE1 or PGE2. These 2 groups also failed to show large elevations in S-T segment which were usually observed in ischemic cats receiving PGF2.alpha. or 0.9% NaCl. Arterial blood samples (i.e., at 5 h) showed significantly increased plasma creatine phosphokinase (CPK) specific activities in MI cats receiving PGF2.alpha. or NaCl, whereas PGE1 and PGE2 infusions prevented significant elevations in plasma CPK during ischemia. Myocardial tissue samples from ischemic cats receiving either PGF2.alpha. or NaCl showed significantly reduced tissue CPK in ischemic myocardial tissue. PGE1 or PGE2 prevented decreases in myocardial CPK activity. Infusion of either E-type 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.