Abstract

Considerable evidence suggests that myocardial injury may occur during reperfusion of the ischemic myocardium. Reactive oxygen species are generated during reperfusion which may play an important role in the genesis of myocardial reperfusion injury. Glutathione (GSH) is an important antioxidant in the heart. A decrease in myocardial GSH content has been observed during ischemia and reperfusion of the ischemic myocardiijm. We hypothesized that this depletion of GSH may be detrimental to the ability of the ischemic myocardium to protect itself against reactive oxygen species during reperfusion.In this study, anesthetized open chest pigs were subjected to coronary occlusion for 45 minutes and 2 hours reperfusion. Myocardial GSH was experimentally depleted by pretreatment with buthionine sulfoximine (BSO), a potent inhibitor of cellular GSH synthesis, and was augmented by intravenous administration of GSH. For ultrastructural study multiple subepicardial biopsies 3 mm deep were taken from myocardium supplied by the occluded artery. The biopsies were processed by routine procedures. Thin sections were stained with uranyl acetate and lead citrate and examined with a Philip EM 300 electron microscope.

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