Calcium-shifts in anoxic cardiac myocytes. A cytochemical study.
Cultivated heart muscle cells from adult rats were exposed to anoxia in a substrate-free Tyrode solution at constant pH. It has been shown previously that in this system anoxic changes of metabolism and morphology develop gradually during the first 60 min. In this study, intracellular Ca2+ localization was pursued cytochemically. Under aerobic control conditions, Ca2+-deposits are only detected along the sarcolemma and T-tubules. Under anoxia the pattern changes gradually. During the first 60 min, the number of sarcolemmal deposits is transiently increased and single deposits appear inside mitochondria. After 90 and 120 min of anoxia, an increasing number of cells have lost their ability of sarcolemmal Ca2+ binding, but exhibit clustered deposits in single mitochondria. These cells are hypercontracted, often contain condensed myofibrillar masses and are covered with large sarcolemmal protrusions, indicating that they are irreversible injured. Loss of sarcolemmal Ca2+ binding ability seems to be a crucial event on the edge of the development of irreversible injury. Since the sarcolemmal Ca2+-deposits in normal cells are believed to be causally related to a binding of Ca2+ to anionic phospholipids, a decrease of Ca2+ affinity of these phospholipids and a change in the sarcolemmal phospholipid composition may be considered as causes for the disappearance of sarcolemma-bound Ca2+.
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D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology; D005260:Female; D006651:Histocytochemistry; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D008854:Microscopy, Electron; D009206:Myocardium / Q000473:pathology* / Q000648:ultrastructure; D010100:Oxygen / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D010100:Oxygen; D002118:Calcium