Metabolic changes in heart muscle during anoxia

¹ Department of Medicine, Washington University School of Medicine, and the Washington University Medical Service, Veterans Administration Hospital, St. Louis, Missouri

The studies reported deal with the effects of varying periods of complete myocardial anoxia on the concentrations of reduced and oxidized diphosphopyridine nucleotide, reduced and oxidized triphosphopyridine, glycogen, adenosine triphosphate, hexose monophosphate, phosphocreatine and inorganic phosphorus in heart muscle. Oxygen lack leads to rapid dephosphorylation of high energy phosphate compounds and to the formation of inorganic phosphorus. The decline of adenosine triphosphate in heart muscle was more rapid than the diminution in the Qo₂ of heart muscle slices reported previously. There was considerable glycogenolysis. The rate of glycogen breakdown did not appear to depend upon the amount of glycogen present in heart muscle until very low levels were reached. Prior to the onset of anoxia, most of the diphosphopyridine nucleotide was in its oxidized form. This oxidized form of diphosphopyridine nucleotide and reduced triphosphopyridine nucleotide decreased with time, while reduced diphosphopyridine nucleotide increased. The total concentration of diphosphopyridine nucleotides in heart muscle diminished.