Anoxic injury of adult cardiac myocytes.
Cultured adult cardiocytes were exposed to anoxia. The initial decrease of high-energy phosphates was accompanied by a moderate release of cytosolic enzymes and morphological changes: the appearance of sarcolemmal 'microblebs' (approximately 1 micron in diameter) and an increase of subsarcolemmal vesicles. At ATP levels above 2 mumol/gww, metabolic and morphological alterations were reversible. Probably the sarcolemmal changes are causally related to the loss of macromolecules from reversibly injured cells. At ATP levels below 2 mumol/gww, an increasing number of cells become irreversibly hypercontracted. In these cells cytoplasmic masses are protruded into large 'macroblebs' (10-30 micron in diameter), however sarcolemmal continuity is preserved. Thus, enzyme release, irreversible contracture and cytolysis do not occur simultaneously in anoxic isolated cardiocytes.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002470:Cell Survival; D002478:Cells, Cultured; D006352:Heart Ventricles / Q000166:cytology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D008854:Microscopy, Electron; D009206:Myocardium / Q000166:cytology*; D010100:Oxygen / Q000494:pharmacology; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains
D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D008291:Malate Dehydrogenase; D010100:Oxygen