Role of ATP metabolites in induction of incomplete recovery of cardiac contractile force after hypoxia.

The present study was designed to elucidate metabolic factors related to reoxygenation-induced recovery of cardiac contractile force after a period of hypoxia, from the view point of energy metabolism in the myocardium. Rabbit hearts were perfused for 20 mins under various degrees of hypoxic conditions, followed by 45 mins of reoxygenation. Hypoxia induced a rise in resting tension, a cessation of cardiac contractile force, a depletion of high energy phosphates, an increase in tissue calcium and an increase in UV absorbance of the perfusate. High performance liquid chromatography analysis of the perfusate indicated that the increase in UV absorbance of the perfusate was attributed to the release of ATP metabolites from the perfused heart. Reoxygenation-induced recovery of cardiac contractile force after 20 mins of hypoxia was predicted by the degree of the rise in resting tension at the final period of hypoxia. The recovery was related to the level of high energy phosphates in the reoxygenated heart as well as the loss of ATP metabolites from the heart but not to the tissue calcium content. The loss of ATP metabolites also correlated with myocardial ATP levels at 45 mins of reoxygenation and a rise in resting tension at 20 mins of hypoxia. The results suggest that loss of ATP metabolites is a vital step in the induction of incomplete recovery of cardiac contractile force after hypoxia.