Experimental studies of the electrocardiographic effect of potassium solution on a toad's heart in the presence of insulin and glucose.

tion on the damaged area of the heart surface , we noted the following results'). Immediately after injury, the ST-elevation was, of course, recorded in the direct unipolar electrocardiogram taken from the injured heart surface . This elevation of the ST-segment was not eliminated even when potassium-free solution was poured on the injured region. As time passed, however, it did not make the ST-elevation whereas the normal Ringer's solution did. Thereafter it was necessary to use samples of higher concentration to produce the ST-elevation as the course progressed ; the concentration of potassium solution was higher to make the ST-elevation. In other words, there exsists a kind of threshold of potassium concentration to produce the ST-elevation and its value rises as time passes after injury. These findings are explained by the supposition that the intracellular potassium was gradually restored after injury, so that the higher concentration was needed to produce the ST-elevation. As the course of the change in the ST-deviation progressed, there came a transient phenomenon, that in order to produce the ST-elevation a higher concent ration of potassium was needed than the normal threshold level seen in an intact heart; the threshold level of potassium was temporarily higher than normal at the end of recovery. It is, therefore, considered that the injured heart cell may take up potassium more than normal at recovery. That the ratio of intra to extracellular potassium concentration exerts an influence upon the ST-deviation, was shown in the previous experiment.