In isolated rabbit myocardium, potassium efflux during brief anoxia is excitation-dependent and dissociable from contraction and energetic state.
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Quiescence attenuates anoxic potassium loss independently of energetics in rabbit myocardium; leaves open whether excitation-dependence offers in vivo cardioprotective targets.
Cellular high-energy phosphate levels and 42K exchange were studied in isolated, interventricular rabbit septa at 28 degrees C. Septa were perfused with a modified Tyrode solution that contained glucose as the metabolic substrate. Anoxia was induced by switching to solution equilibrated with N2-CO2 gas. Potassium lost during anoxia by increased efflux from the cells was measured by 42K. Whole tissue levels of ATP, ADP, phosphocreatine, and total creatine were determined. The effects of 20-min anoxic stresses were evaluated in each of four groups of septa: 1) control (perfused with regular solution and paced at 42 excitations/min; 2) E-C uncoupled (by perfusing with solution containing 50 micron Ca2+); 3) quiescent (spontaneous contraction rate less than 1/min); and 4) perfused with high glucose solution (20 mM). Compared to the control group, only quiescence significantly decreased the potassium loss during anoxia; the cellular energetic state was well maintained during stress by both E-C uncoupling and quiescence. The results indicate that the increase in potassium efflux during brief anoxic stress is largely excitation dependent and can be dissociated from contraction and cellular energetic state.
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Rau et al. (1978) studied this question.
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