Irreversible damage to sarcolemmal Ca2+ transport in myocardial ischemia.
Perfusion of isolated rat hearts for 10 min with substrate-free hypoxic medium resulted in a depression of sarcolemmal Na+-dependent Ca2+ uptake, Ca2+-stimulated ATPase, ATP-dependent Ca2+ uptake and Na+-K+ ATPase in sarcolemma. Reoxygenation of these hearts resulted in a further depression of all these activities. Na+-induced Ca2+-efflux was unaffected in vesicles of hearts subjected to hypoxia-reoxygenation. Developed contractile force and resting tension in hypoxic hearts were 15% and 400% of control values, respectively, while reoxygenation was associated with a slight recovery of developed contractile force and the resting tension was lowered appreciably but remained elevated. Because sarcoplasmic reticular Ca2+ uptake and mitochondrial Ca2+ uptake were depressed under similar conditions, cellular injury due to hypoxia-reoxygenation was not specific to the sarcolemma. These results indicate that inability of the ischemic heart to recover its function may be associated with defects in Ca2+-transport systems.
D000818:Animals; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D012508:Sarcolemma / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D007473:Ion Channels; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium