Why the study?
Does diphenylhydantoin alter electrophysiological properties and arrhythmias in the canine heart?
Does diphenylhydantoin alter electrophysiological properties and arrhythmias in the canine heart?
Diphenylhydantoin exerts complex, state-dependent electrophysiological effects on the canine heart and demonstrates antiarrhythmic efficacy against digitalis-induced ventricular tachycardia.
Answers are grounded in this paper and cite their sources.
State-dependent effects in canine models support mechanistic studies of digitalis arrhythmias; leaves open human translation.
These studies were designed to examine the electrophysiological effects of diphenylhydantoin (Dilantin) on the heart of awake dogs. Recording electrodes were implanted over the sinoatrial node, bundle of His, and right bundle branch, and studies were performed 2 to 6 weeks following recovery. Diphenylhydantoin (10 mg/kg) increased heart rate, shortened A-V conduction time and had little or no effect on conduction velocity in Purkinje tissue or total ventricular activation time. Similar effects were noted when heart rate was controlled by pacing. Following cardiac denervation, diphenylhydantoin decreased heart and prolonged A-V conduction time. It raised the threshold of atrial and ventricular muscle with no change of refractory periods. In dogs with heart block, it decreased the maximal rate at which the atria would respond to stimulation. When ventricular tachycardia was induced in dogs with heart block, by toxic doses of deslanoside, diphenylhydantoin abolished the ectopic tachycardia and restored the control rhythm.
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Rosati et al. (1967) studied this question.
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