Energy metabolism and enzyme release of cultured adult rat heart muscle cells during anoxia.
An intact preparation of adult ventricular muscle cells was incubated in substrate-free, pH-constant, anoxic Tyrode solution. The time course of metabolic changes was found to depend on the relation of cell number to incubation volume: the smaller the volume, the faster anoxic damage develops. Energy needs decline rapidly during anoxia. Yet glycolytic energy production remains insufficient, since it also declines. Glycogenolysis stops after degradation of only half the glycogen present initially. Release of cytosolic enzymes (LDH, MDH) starts with the initial decrease in high-energy phosphates and proceeds correlated to the actual ATP content (r = -0.98) during the stage of reversible cell injury. An ATP content of 2 mumol/g wet wt. marks a critical threshold, below which more and more cells become irreversibly damaged. In the cell culture system, the anoxic process develops similarly to that of the oxygen deficient organ, however prolonged as in arrested hearts.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D002478:Cells, Cultured; D004734:Energy Metabolism; D006019:Glycolysis; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats
D000227:Adenine Nucleotides; D007770:L-Lactate Dehydrogenase; D008291:Malate Dehydrogenase