Enhanced prostaglandin production in the ischemic-reperfused myocardium by captopril linked with its free radical scavenging action.

Captopril, an angiotensin converting enzyme inhibitor, has been shown to increase prostaglandin production by an as yet unknown mechanism, which this study was designed to explore. Isolated rat heart was perfused by the Langendorff technique for 15 minutes in the presence or absence of captopril. Ischemia was then induced for 60 minutes by terminating the coronary flow, followed by 60 minutes of reperfusion. Our results indicate that captopril stimulated prostaglandin and thromboxane production, but it inhibited malonaldehyde formation. Coronary flow and high energy phosphate compounds were increased, but lactate dehydrogenase and creatine kinase release decreased, demonstrating cardioprotective effects. Captopril also inhibited the production of hydroxyl radical in the heart during reperfusion, suggesting that stimulated prostaglandin production may be linked with the generation of free radicals via the eicosanoid system.