Abstract
These observations raise some interesting practical questions. Is it possible to Increase the therapeutic effects of digitalis and to diminish the toxic effects? The 2 mechanisms appear to be separate and yet to have identical molecular requirements. Perhaps more could be done by altering the conditions in which the drug acts. So far the accidental enhancement of toxicity produced by thiazlde diuretics or occasionally by administration of calcium salts has been more prominent than attempts to minimize arrhythmias by giving extra potassium salts. It is also interesting to ask why the falling heart benefits from the action of digitalis. The failure of Ca movement may be fundamental in the pathogenests of failure: or the action of digitalis may be purely palliative, boosting one part of the mechanism so that defects of another part are temporarily covered. There is still much to be discovered, but the general mode of action of cardiac glycosides is clearer than it has ever previously been.