MECHANISMS INVOLVED IN THE ANTIARRHYTHMIC AND PROARRHYTHMIC EFFECTS OF MAGNESIUM

This paper reports an electrophysiological study on the antiarrhytmic 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 suppleme ntation (group IIA) or a low magnesium diet plus chlortalidone treatme nt 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 ef fective refractory period (VERP) and increased the urinary excretion o f potassium. The infusion of magnesium chloride solution did not affec t 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 sol ution depressed further VFT and plasma potassium and increased VERP. T he acute infusion of potassium chloride solution increased plasma pota ssium and VFT. In group II B, plasma electrolyte levels and electrophy siological variables were not affected. We conclude that the clinicall y demonstrable, antiarrhythmic effect of magnesium infusion can be att ributed to prolonged VERP. Magnesium sulphate infusion, however, produ ced potassium depletion and decreased VFT (a pro-arrhythmic effect). T hese adverse effects can be avoided infusing magnesium chloride soluti ons.