Oxidative Metabolism in Reperfused Myocardium

Abstract

In normal myocardium there exists a close relationship between the oxidative metabolic rate and contractile performance. A number of recent studies in dogs and pigs with experimentally induced regional ischemia have suggested that myocardial oxygen consumption may be disproportionately high compared to contractile function after postischemic reperfusion [1,2]. We have studied myocardial oxidative metabolism after reperfusion in isolated rat hearts perfused retrogradely with erythrocyte-enriched Krebs-Henseleit buffer containing glucose 11 mM and palmitate 0.4 mM bound to albumin 0.4 mM [3]. Fifteen minutes after the onset of reperfusion following 60 minutes of normothermic no-flow ischemia, left ventricular isovolumic pressure development was still severely depressed to 13% of the corresponding value in control hearts without ischemia (p<0.01). However, despite poor recovery of contractile function, myocardial oxygen consumption was only slightly reduced to 87% (NS) when compared to control hearts.