[Mechanisms involved in the antiarrhythmic and proarrhythmic effects of magnesium]

This paper reports an electrophysiological study on the antiarrhythmic and proarrhythmic actions of magnesium chloride and magnesium sulphate intravenous infusions. Magnesium kinetics in control dogs, following a pulse of magnesium chloride or magnesium sulphate, was not affected by the accompanying anion. The experiments were performed with mongrel dogs divided into three groups fed either a normal diet (group I), a low magnesium diet plus chlortalidone treatment and potassium supplementation (group IIA) or a low magnesium diet plus chlortalidone treatment and magnesium sulphate infusion (group II B). In group I, infusion of magnesium sulphate solution decreased plasma sodium, potassium and ventricular fibrillation threshold (VFT), prolonged the ventricular effective refractory period (VERP) and increased the urinary excretion of potassium. The infusion of magnesium chloride solution did not affect VFT, prolonged VERP, QTc, AH and PQ. In this group, sodium chloride or sulphate infusion did not affect the electrophysiological variables but sodium sulphate decreased plasma potassium levels. The group II A was characterized by the decreased levels of potassium and magnesium contents of plasma, lymphocytes and myocardium, decreased VERP and VFT and prolonged QTc. The intravenous infusion of magnesium sulphate solution depressed further VFT and plasma potassium and increased VERP. The acute infusion of potassium chloride solution increased plasma potassium and VFT. In group II B, plasma electrolyte levels and electrophysiological variables were not affected. We conclude that the clinically demonstrable, antiarrhythmic effect of magnesium infusion can be attributed to prolonged VERP. Magnesium sulphate infusion, however, produced potassium depletion and decreased VFT (a pro-arrhythmic effect). These adverse effects can be avoided infusing magnesium chloride solutions.