Abstract
When succinate is administered to the heart-lung prepn. of the dog at sufficiently high rates (0.2 g. or more of unhydrated succinate anion per kg. heart-lung system per min.) the phosphocreatine concn. in the myocardium declines markedly and the heart goes into failure. The concn. of ATP declines to a lesser extent or remains unchanged. Heart failure in the heart-lung prepn. caused by pentobarbital and chlorobutanol is intensified by succinate. These findings are discussed in the light of existing information on the coupling of succinate oxidation with phosphorylation and on the metabolism of cardiac tissue poisoned with anesthetics.