Abstract
Summary
When succinate is administered to the heart-lung preparation of the dog at sufficiently high rates (0.2 g or more of un-hydrated succinate anion per kg heart-lung system per minute) the phosphocreatine concentration in the myocardium declines markedly and the heart goes into failure. The concentration of ATP declines to a lesser extent or remains unchanged. Heart failure in the heart-lung preparation 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.
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