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Digitalis: ions, inotropy and toxicity.

As we enter the third century of the clinical use of digitalis, much remains to be learned about this useful but relatively toxic family of drugs. Current thinking about basic mechanisms of cardiac glycoside action at the cellular level can be traced to the observation of Schatzmann that transmembrane active transport of Na+ and K+ is potently and specifically inhibited by digitalis.1 Schatzmann used human red blood cells in his studies, and it is of interest that this fundamental finding, presented 25 years ago, has now been extended to potential clinical usefulness by the report of Loes and his colleagues . . .