Changes in the erythrocyte potassium in patients with cardiac failure treated with digitalis.

T HAS BEEN SHOWN that cardiac glycosides inhibit the re-entry of potassium from the plasma into cold-stored erythrocytes and that the normal influx of potassium into the cells from the plasma of fresh blood incubated at 37#{176} can be almost abolished by the presence of cardiac glycosides (1). The normal efflux of potassium from the cells under these conditions is not inhibited and the cells show a net loss of potassium. The concentrations of glycosides required to produce 50 per cent inhibition vary from 4 X 10 molar in the case of ouabain to 1.2 X 10 molar in the case of digitoxin (2). There is some evidence that adrenal steroids cause an increase in erythrocyte potassium in vivo due to an increase in potassium influx into the cell (3). In cardiac failure the level of aldosterone in the blood is increased and returns towards normal following cardiac compensation. There are, therefore, two possible mechanisms which might be expected to produce a fall in the erythrocyte potassium level in patients with cardiac failure treated with glycosides. In patients under treatment for cardiac failure the diminished production of adrenal steroids associated with the improvement in the cardiac condition and the direct action of cardiac glycosides on the erythrocytes might both be expected to cause a drop in the erythrocyte potassium.