Normal Oxidative Phosphorylation in Mitochondria from the Failing Heart

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Abstract
Oxidative phosphorylation was measured polarographically in mitochondria isolated from normal ventricles and from the ventricles of guinea pigs and cats with experimental heart failure produced by constriction of the aorta or pulmonary artery. The presence of heart failure was proved by the study of myocardial mechanics in vitro, by cardiac catheterization, and by postmortem examination. Mitochondria from failing ventricles had normal oxidative phosphorylation, and P-O ratios, respiratory control, oxygen consumption and ATPase activity did not differ from those of mitochondria from normal hearts. Results were the same whether incubations were performed at 25° or 37°C and whether glutamate or pyruvate and malate were used as the substrate. Mitochondria showed functional deterioration, probably due to fatty acid accumulation, when incubated for more than 10 min at 37°C or when isolated from hearts made hypoxic in vivo for as little as 3 min. The results of this study suggest that decreased myocardial contractility in experimental heart failure is not due to an intrinsic defect in mitochondrial function.