Abstract
Summary
Diphenylhydantoin (DPH) in doses as low as 10 mg/kg produces significant and long lasting depression of the accelerator response to pre- and postganglionic stimulation. The response to isoproterenol was not affected when neurally-induced acceleration was diminished. Only after the very large dose of DPH was the isoproterenol response diminished and it required a much longer period to develop than the reduction in the neural effect. It was concluded that diminution in nerve-induced acceleration by DPH is due to a neural depressant effect rather than an effect on beta-adrenergic receptors. There did not appear to be any correlation between the action of the drug to decrease blood pressure and heart rate and the action of the drug to depress the response to accelerator nerve stimulation. Since the neural depressant action occurred with doses which are also effective against digitalis-induced arrhythmia, this antiarrhythmic effect of DPH seems to be associated with depression of adrenergic nervous activity.
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