Akinori Satoh

Role of autonomic nervous activity in the antiarrhythmic effects of magnesium sulfate in a canine model of polymorphic ventricular tachyarrhythmia associated with prolonged QT interval.

Abstract: This study was performed to examine the role played by the autonomic nervous system in the antiarrhythmic effects of magnesium sulfate (Mg++) in a canine model of polymorphic ventricular tachyarrhythmia facilitated by anthopleurin-A and a slower heart rate induced QT interval prolongation. In 6 experiments, complete atrioventricular block was created to control the heart rate and bradycardia at 800- to 1500-ms cycle lengths was applied for 60 sec before and after drug-induced autonomic block. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and activation-recovery intervals (ARI) were measured. Before drug-induced autonomic block, polymorphic ventricular tachyarrhythmia developed in all 6 experiments during bradycardia before but not after the administration of Mg++ (0.2 ml/kg intravenous bolus). During drug-induced autonomic block, triggered premature activity decreased without significant changes in underlying dispersion of repolarization and polymorphic ventricular tachyarrhythmia developed during bradycardia in 1 experiment. Administration of Mg++ during drug-induced autonomic block eliminated premature activity and polymorphic ventricular tachyarrhythmia during bradycardia. The distribution of left ventricular (LV) and right ventricular repolarization and dispersion of transmural repolarization were analyzed before and 60 sec after Mg++ administration during ventricular pacing at 80 bpm. Mg++ caused a modest shortening of ARI at all sites before and after drug-induced autonomic block. Since ARI shortening was greater at the mid-myocardial sites than at other LV sites, Mg++ decreased transmural ARI dispersion from 77 ± 16 to 46 ± 21 ms before drug-induced autonomic block and from 79 ± 7 to 51 ± 16 ms after drug-induced autonomic block. The antiarrhythmic effects of Mg++ in this model of long QT syndrome were attributable to its direct pharmacological properties and not to changes in ambient autonomic nervous activity. The blockade of sympathetic activity decreased the incidence of premature events and partially suppressed polymorphic ventricular tachyarrhythmia in this model.