Abstract
The rates of incorporation of Pi32 into the [gamma]- and [beta]-phosphates of myocardial ATP were compared in normal dogs and in dogs with right ventricular hypertrophy or chronic congestive heart failure produced by pulmonary artery ligatures. Reproducible control values were obtained in right ventricles after injection of Pi32 into the vena cave and extirpation of the beating heart at 5 min. or after injection of Pi32 and K citrate into the aorta and instant removal of the arrested heart. Administration of DNP produced significant changes in the labeling of ATP phosphates. In the failing hearts, there were no significant changes in the labeling of the [gamma]-phosphate of ATP, a rough index of oxidattve phosphorylation and Pi32-ATP exchange, or in the relative labeling of the [beta]-phosphate, an index of myokinase activity. Consideration of these findings, together with the falls in CrP and ATP noted previously, suggests that a combined decrease in mitochondrial oxidative phosphorylation and myofibrillar ATPase may characterize the failing hearts.