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• W2099644329 abstract "Parasympathetic neural activity modulates some ventricular arrhythmias in man. Therefore, a canine model of arrhythmias produced by the interaction of halothane and catecholamines was used to study the effects of vagal stimulation on the induction of ventricular fibrillation. The dose of catecholamine required to induce ventricular fibrillation was determined during a constant heart rate. Vagal stimulation reversibly raised the norepinephrine dose that produced ventricular fibrillation from 16.4 ± 2.4 to 30.0 ± 3.8 μg (p < 0.001, n = 10), and the epinephrine dose from 15.5 ± 2.0 to 22.5 ± 2.6 μg (p < 0.001, n = 5). Following atropine, vagal stimulation failed to raise the threshold dose of norepinephrine (16.8 ± 2.4 vs.18.3 ± 3.3 μg, nonsignificant, n = 6) or epinephrine (15.5 ± 2.0 vs. 16.0 ± 2.3 μg, nonsignificant, n = 5). Ligation of the cervical vagus nerves did not affect the epinephrine threshold dose (16.3 ± 3.3 vs. 17.5 ± 2.7 μg, nonsignificant, n = 5). Following elevation of basal vagal tone by morphine premedication, the norepinephrine threshold dose of 53.0 ± 9.2 μg declined by a nonsignificant amount to 46.5 ± 11.5 μg after vagotomy (nonsignificant, n = 5). Thus resting vagal tone does not prevent catecholamine–halothane-induced ventricular fibrillation, whereas increasing vagal tone by electrical stimulation substantially protects against this arrhythmia. The protection is mediated through a muscarinic cholinergic receptor.Key words: ventricular arrhythmias, vagal tone." @default.
• W2099644329 created "2016-06-24" @default.
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• W2099644329 date "1989-07-01" @default.
• W2099644329 modified "2023-10-16" @default.
• W2099644329 title "The protective effect of vagus nerve stimulation on catecholamine–halothane-induced ventricular fibrillation in dogs" @default.
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• W2099644329 doi "https://doi.org/10.1139/y89-127" @default.
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