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.