Cell to cell interactions contributing to the "oxygen paradox".
Intact rat hearts demonstrate a sudden release of cytoplasmic proteins when they are subjected to reoxygenation following anoxic injury (oxygen paradox). Reoxygenation enzyme release is associated with cellular swelling and contraction band necrosis. Reoxygenation damage is reduced by mitochondrial inhibitors, and DMSO which prevent cellular hypercontracture. An oxygen paradox also occurs during reperfusion of ischemic hearts but has not been reported to occur in isolated adult myocyte preparations. The absence of cell interactions in reoxygenated isolated cell preparations could allow unrestrained contracture to occur without transmission of disruptive forces to cell membranes. Other equally plausible explanations have not, however, been ruled out. Future studies will be required to establish the pathogenesis of the oxygen paradox and explain its apparent absence in the isolated adult myocyte model of cell injury.
D000818:Animals; D002450:Cell Communication; D002469:Cell Separation; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology; D004140:Dinitrophenols / Q000494:pharmacology; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology; D008929:Mitochondria, Heart / Q000473:pathology; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism* / Q000648:ultrastructure; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D012508:Sarcolemma / Q000473:pathology; D013997:Time Factors
D004140:Dinitrophenols; D010100:Oxygen