Preservation of resting potential by magnesium in hypoxic canine cardiac cells.

This study was designed to test the hypothesis that Mg++ prevents the electrophysiologic changes caused by hypoxia in cardiac cells. Canine right ventricular false tendons (32 hearts) were pinned to the floor of a tissue bath and suffused with physiologic solution. Microelectrodes recorded the spontaneous action potentials. The isolated tissue was exposed to a hypoxic solution (PO2 less than 50 mm Hg) containing either normal [Mg++] (0.85 mmol/l) or high [Mg++] (3.4 mmol/l). Hypoxia with normal [Mg++] caused increased firing rate (+40%), depolarization of the resting (maximum diastolic) potential (from-72 to -55 mV), and reduction in amplitude (from 88 to 76 mV). The depolarization, reduction in amplitude, and most of the increased firing rate were completely blocked when [Mg++] was elevated to 3.4 mmol/l; propranolol (10 mg/l) blocked the residual increase in firing rate.