Why the study?
Does intravenous thioridazine alter sinusal automaticity, myocardial excitability, and auriculoventricular conduction in dogs?
Does intravenous thioridazine alter sinusal automaticity, myocardial excitability, and auriculoventricular conduction in dogs?
Thioridazine exhibits quinidine-like electrophysiological properties that prolong auriculoventricular conduction and increase atrial refractory period, providing a mechanistic basis for its clinical cardiotoxicity.
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Supports quinidine-like effects in dogs; leaves open human cardiotoxicity translation.
The effect of thioridazine on sinusal automaticity, myocardial excitability and auriculoventricular conduction have been studied in dogs by measuring the spontaneous heart rate, the effective refractory period of the atrial contractile tissue, the time of auriculonodal and infrahisian conduction. Chloralose anaesthetized dogs were administered 10 mg/kg thioridazine hydrochloride via intravenous route. While sinusal automaticity was not altered, conduction times were prolonged in the suprahisian and mainly the infrahisian part and the atrial refractory period increased. These effects are related to quinidine-like properties and consistent with cardiotoxic effects previously reported in clinical practice.
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Descotes et al. (1979) studied this question.
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