Abstract

Potassium fluxes in both directions have been measured in the dog heart in situ. Influx and efflux are estimated to be 0.75 mEq/kg of wet heart weight per minute. Potassium influx is increasingly inhibited as the doses of ouabain and 3-acetyl strophanthidin increase; with doses causing irregularities this could reach 50% inhibition. Increase in heart rate by driving the heart electrically during cardenolide action has small effects on influx. Potassium efflux is decreased with therapeutic doses, more with the smaller doses than with higher ones. Since cardiac acceleration increases potassium efflux in the cardenolide treated heart, a part of this difference could be due to the faster heart rate produced by the cardenolides. Still higher doses increased efflux above the control level and irregularities occurred. The intracellular amount of potassium calculated from the fluxes is increased during the positive inotropic action of small doses of the cardenolides and decreased during the positive inotropic action of higher doses. Irregularities produced by toxic doses of the cardenolides occur shortly after or at the beginning of the major decrease in intracellular potassium; the heart rhythm reverts to normal at the time of the lowest intracellular potassium concentration. This indicates that a decrease of the intracellular potassium concentration is not the cause of either these therapeutic or toxic effects of the cardenolides; these effects are more likely to result from changes in membrane properties.