Enhanced sympathetic activity as a mechanism for cardiac glycoside toxicity in hypomagnesemia

Hypomagnesemia was induced in dogs by administration of furosemide (20 mg/kg/day) for 7 days. Following replacement of a concomitant loss of potassium, ouabain was infused at 1 microgram/kg/min until death. The inotropic response, sustained ventricular arrhythmias, and death all occurred at significantly lower ouabain doses in hypomagnesemic animals than in normomagnesemic dogs. Additionally, hypomagnesemic dogs exhibited an abrupt sympathetic discharge which could be interrupted by bilateral ablation of the stellate ganglia. These results suggest that the neuroexcitatory effects of cardiac glycosides are enhanced during hypomagnesemia.