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.