Ionic movements and irreversible anoxic damage.
Myocyte hypercontracture can be produced by adding Ca2+ to calcium-intolerant myocytes. A similar morphologic change occurs in Ca2+-free media when anoxic, ATP-depleted myocytes are reoxygenated or when respiring myocytes are lysed with digitonin. Hypercontracture in Ca2+-free media is abolished by rotenone, an inhibitor of NADH-linked respiration. Rotenone-treated, digitonin-permeabilized myocytes were used to examine the effects of MgATP, pCa, and respiration on hypercontracture. In the absence of Ca2+ (pCa 8.5), hypercontracture occurred at low MgATP but not when ATP was increased above 1 mM. At high MgATP (1-10 mM), hypercontracture was Ca2+-dependent. Succinate did not cause hypercontracture in the absence of added MgATP, but it shifted the concentration dependence for Ca2+-independent hypercontracture to lower values by regenerating ATP.
R A
RA
Altschuld
W C
WC
Wenger
G P
GP
Brierley
D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D002463:Cell Membrane Permeability / Q000187:drug effects; D002469:Cell Separation; D004072:Digitonin / Q000494:pharmacology; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D007473:Ion Channels / Q000378:metabolism*; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D010101:Oxygen Consumption; D051381:Rats
D007473:Ion Channels; D004072:Digitonin; D002118:Calcium