"Protective" action of diphenylhydantoin on canine Purkinje fibers during hypoxia.

Intracellular microelectrode recording techniques were used to elucidate the mechanism of antiarrhythmic action of diphenylhydantoin (DPH) in isolated canine Purkinje fibers during periods of hypoxia induced by 95% nitrogen-5% carbon dioxide. Hypoxia caused a fall in resting and action potential amplitude and in the maximum rate of rise (Vmax) of phase zero of the Purkinje fiber action potential. In six experiments, the mean time to one-half of control phase zero Vmax was 52 ± 10.4 minutes (mean ± S.E.) during hypoxia and 110 ± 15.1 minutes during hypoxia and intervention with DPH (10-8 M) (P < .005). DPH (10-7 M) transiently improved phase zero Vmax and conduction when these characteristics were depressed during hypoxia. It is suggested that the ability of DPH to delay significantly the decrease in Vmax of phase zero of the Purkinje fiber action potential induced by hypoxia may partially explain its effectiveness in abolishing ventricular arrhythmias resulting from occlusion of coronary arteries.