Potassium exchange and mechanical performance in anoxic mammalian myocardium.

Mechanical performance and 42K exchange were studied during anoxia in isoalted, arterially perfused, interventricular rabbit septa at 42 beats/min and 28 degree C. The septa were perfused at 1.8 ml/min per g with a modified Tyrode solution having dextrose as the metabolic substrate. Developed tension declined to 16% of preanoxic control values during 60 min of anoxia, and returned to 65% of control during a 60-70 min recovery. Anoxia induced net potassium losses of 31+/-2, 53+/-2, and 90+/-14 mmol K+/kg dry tissue (means+/-SE) during 20, 40, and 60 min of anoxic stresses, determined by tissue probe analysis after asymptotic labeling. Potassium losses attributed to increased efflux of the ion from the cells during 20, 40, and 60 min of anoxia were determined from effluent analyses to be 32+/-4, 60+/-6, and 98+/-11 mmol K+/kg dry wt. Potassium loss began within seconds of the onset of anoxia and reoxygenation immedaitely reversed the potassium loss. These data indicate that 1) function of the membrane Na-K pump is maintained through 60 min of anoxia with the entire net potassium loss attributable to increased efflux from the cells, 2) anoxia decreases the rate of exchange of potassium after recovery, and 3) the cell membrane appears to be the rate-limiting site of potassium efflux during anoxia.