On the therapeutic mechanism of Mg2+ in digitoxic arrhythmias and the role of cardiac glycosides in Mg depletion.

In 9 (of 17 attempted) experiments (8 aborted due to premature tissue death), transmembrane electrical activity was recorded from canine false tendons superfused with Mg-free Tyrode's solution to simulate hypomagnesemia. Oscillatory after-potentials (OAP) developed similar to those seen after exposure to 2 X 10(-7) M ouabain, a short-lasting (0.5-1 time the duration of an action potential) OAP that often reached threshold superimposed on a long-lasting (3-4 times as long as the short) OAP. Both forms of OAP were shown to be Ca2+-dependent, as both were prevented by 10(-7) M nifedipine, but only the short OAP were abolished by nifedipine once they had appeared, while high (5 mM = 10 times normal) Mg2+ both prevented and terminated short and long OAP in digitoxic preparations. Results suggest that cardiac glycosides may deplete Mg from the myocardium. The mechanism of the therapeutic action of Mg2+ in digitalis intoxication is discussed in light of its involvement in Ca2+ sequestration by the sarcoplasmic reticulum.