Isolated hearts from copper-deficient rats exhibit improved postischemic contractile performance.

Dietary copper deficiency affects a number of enzymes, the function of which may influence the outcome of myocardial ischemia-reperfusion injury. Male weanling rats were fed diets that were adequate (> 5 mg/kg) or deficient (< 1 mg/kg) in copper. After 4 wk, the rats' hearts were isolated and used to study the effects of ischemia-reperfusion on intraventricular developed pressure (DevP), positive and negative rates of intraventricular pressure change (+dp/dt and -dp/dt) and release of lactate dehydrogenase and creatine kinase from the heart. The ischemia-perfusion protocol included a 15-min equilibration period, 30 min of warm, total ischemia and reperfusion for 30 min. Preischemic hearts from copper-deficient rats produced lower DevP than hearts from copper-adequate rats at all levels of preload. However, postischemic recovery of DevP was significantly greater in the hearts of the copper-deficient group. Furthermore, the postischemic patterns of lactate dehydrogenase and creatine kinase release in the two groups were significantly different. These findings indicate that, although dietary copper deficiency adversely affects a number of enzymatic systems, the functional recovery of hearts subjected to ischemia-reperfusion injury is improved when the diet is restricted in copper.