A.: Influence of ouabain on intracellular sodium and potassium concentrations in the rabbit myocardium

One current concept of the action of the carclio-active glycosides is based on experiments which show that they reduce the intracellular potassium (K+) concentration in myocardium (Hajdu and Leonard, 1959), red blood cells (Schatzmann, 1953) and skeletal muscle (Schatzmann and \Vitt, 1954). In certain concentrations these drugs reduce myocardial K ’ by blocking potassium influx without affecting its efflux (Schreiber, 1956; Rayner and Weatherall, 1957; Vick and Kahn, 1957). A relationship between heart rate and the onset of cardioactive drug action has been reported (Wilbrandt et at., 1953; Sanyal and Saunders, 1958). This suggests that increased muscle activity may facilitate the mechanism by which the glycosides improve the contractility of heart muscle. There is evidence that the con-centration and fluxes of the K+ ion may be related to the level of myocardial activity. Schreiber (1956) and Rayner and Weatherall (1957) ob-served that K+ efflux may be increased by in-creased myocardial activity and Wilde and O’Brien3 (1953) reported that an increased out-flux of potassium was associated with each action potential. Vick and Kahn (1957) observed that in guinea-pig hearts stimulated at rates above the intrinsic rhythm a K+ loss occurred. The evi-dence that both the cardioactive glycosides and increased heart rate produce a net loss of K+ from myocardium and an increase in contractile force has led Hajdu and Leonard (1959) to postulate that “potassium loss is causally related to the increase in contractility. ” Several investi