Myocardial contractile function during ischemia and hypoxia.
There is good evidence that elevated [Ca2+]i, produced by an influx of Ca2+ in exchange for Na+, is the underlying pathology in reperfusion or reoxygenation damage. Further measurements of [Na+]i and [Ca2+]i during ischemia and reperfusion, coupled with information about metabolic levels, are needed to confirm or refute this hypothesis. Contributions to cell damage by other mechanisms, e.g., oxygen free radicals, certainly cannot yet be excluded.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001696:Biomechanical Phenomena; D002118:Calcium / Q000378:metabolism; D002451:Cell Compartmentation; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000503:physiopathology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D009210:Myofibrils / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D011485:Protein Binding; D012964:Sodium / Q000378:metabolism
D010758:Phosphorus; D000255:Adenosine Triphosphate; D012964:Sodium; D002118:Calcium