Intracellular Ca2+ shifts during the Ca2+ paradox.
The distribution of Ca2+ is assessed cytochemically in isolated rat hearts subjected to low Ca2+ environment with and without subsequent reexposure to normal external Ca2+. The same is done for isolated rat cardiac myocytes. The inclusion of 15 microM Ca2+ in the perfusate predisposes hearts to a partial paradox with increasing intensity towards the subepicardium. In affected areas, morphologically characterized by deviation of the lamina externa from the surface coat-sarcolemma and separation of some regions of the intercalated disk, the sarcolemma was devoid of Ca2+ deposits. Upon reperfusion, irreversible contracted cells with ruptured sarcolemma showed accumulation of Ca2+ precipitate in mitochondrial matrices. In non-affected cells (subendocardium) sarcolemmal Ca2+ was normal and mitochondria were virtually devoid of Ca2+ precipitate. Isolated myocytes were insensitive to Ca2+ deprivation and/or repletion and no Ca2+ shifts were demonstrated. These observations suggest a role for sarcolemma-bound Ca2+ in the integrity of this membrane.
D000818:Animals; D001826:Body Fluids / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002469:Cell Separation; D006651:Histocytochemistry; D007365:Intercellular Junctions / Q000648:ultrastructure; D007424:Intracellular Fluid / Q000378:metabolism*; D008854:Microscopy, Electron; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D012508:Sarcolemma / Q000187:drug effects*; D013997:Time Factors
D002118:Calcium