Absence of reoxygenation damage in isolated heart cells after anoxic injury.
Cultured adult cardiac myocytes were exposed to anoxia under substrate-free conditions and then reoxygenated. When comparing the oxygen deficient organ to the anoxic cell culture, we see that metabolic changes in the latter system proceed in a similar, yet prolonged manner, as in arrested hearts. Release of cytosolic enzymes starts with minor energetic disturbances and proceeds closely correlated to the actual ATP level. Below 2 mumol ATP/gww, an increasing number of cells becomes irreversibly damaged, above this level, 30 min reoxygenation leads to extensive recovery of the whole preparation. The results indicate that leakage of cytosolic enzymes during the early stage of anoxia is due to a gradual protein release from the individual cells and is related to reversible membrane alterations. Reoxygenation does not induce changes considered typical of the 'oxygen paradox'. Since mechanical cell-cell interactions are absent in this model, it is suggested that aggravation of tissue damage in heart tissue reoxygenated late is mainly caused by mechanical forces.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002478:Cells, Cultured; D004734:Energy Metabolism; D005260:Female; D008928:Mitochondria; D008929:Mitochondria, Heart / Q000378:metabolism*; D008933:Mitochondrial Swelling; D008954:Models, Biological; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism* / Q000648:ultrastructure; D010100:Oxygen / Q000502:physiology*; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D012518:Sarcomeres / Q000648:ultrastructure
D000255:Adenosine Triphosphate; D010100:Oxygen