Cardiomyopathic and healthy acidotic hamster hearts: mitochondrial activity may regulate cardiac performance.

A 50% decrease in adenine nucleotides and a 60% decrease in adenosine triphosphate concentration was found in glucose perfused myopathic Syrian hamster heart (240 days old) whereas there was an 18% decrease and 40% decrease respectively in acidotic healthy Syrian hamster heart re-equilibrated with a physiological medium. Correspondingly, there was a 60% decrease in cardiac performance with both models. Developed pressure fell when the phosphorylation potential decreased to less than or equal to 2; however, the heart recovered if mitochondrial activity was activated. If a substrate such as pyruvate or ribose was used with either model cardiac performance returned to near normal, although adenine nucleotide and adenosine triphosphate concentrations were further depressed. With glucose as substrate cardiomyopathic hearts, healthy acidotic hearts, and healthy acidotic hearts re-equilibrated with glucose as substrate had low pyruvate concentrations; limited availability of pyruvate depressed mitochondrial activity. Like the myopathic hearts the re-equilibrated acidotic hearts had high myocardial pyruvate concentrations, above normal ratios of phosphocreatine to creatine, and near normal oxygen consumption, developed pressure, dP/dt, and cyclic adenosine monophosphate concentrations when re-equilibrated with a medium containing pyruvate or ribose as substrate, although adenosine triphosphate and adenine nucleotide concentrations were severely depressed. When adenosine triphosphate values fell from 24 to 2 mumol X g-1 dry weight in the pyruvate or ribose perfused and normal functioning heart the heart stopped beating with no progressive fall in performance before termination of the metabolic processes.