Key result
IV nifedipine shortens RV action potential duration and refractoriness in acebutolol-pretreated canine models.
Why the study?
The basic cardiac effects of nifedipine can be altered by catecholamine release, necessitating study of its direct effect on right ventricular electrophysiology after beta-adrenergic blockade.
Does intravenous nifedipine decrease the action potential duration and refractoriness in the right ventricle of the dog heart in situ after beta-adrenergic blockade?
Population
Dog heart in situ pretreated with acebutolol under pentobarbital anaesthesia
Comparison
Intravenous nifedipine 30 microgram/kg vs baseline after beta-adrenergic blockade
Design
Preclinical electrophysiological study using monophasic action potential recordings and programmed electrical stimulation
Authors
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Nifedipine may shorten canine ventricular repolarization independently of beta-adrenergic effects; leaves open translation to human electrophysiology and arrhythmia risk.
Does intravenous nifedipine decrease the action potential duration and refractoriness in the right ventricle of the dog heart in situ after beta-adrenergic blockade?
Nifedipine directly decreases action potential duration and refractoriness in the right ventricle of the dog heart in situ, independent of sympathetic reflex mechanisms.
Amlie et al. (1979) studied this question. Nifedipine was evaluated on Times for 50 and 90 per cent repolarization of the monophasic action potential and effective/functional refractory period. Intravenous nifedipine (30 µg/kg) decreased the action potential duration and refractoriness of the right ventricle in dogs pretreated with acebutolol.
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