Influence of Digitalis on the Sensitivity of the Cardiac Vagus Endings

Abstract

The work of Heymans 1 , 2 on the mechanism of the bradycardia of digitalis seems to dispose of the older theory that this drug stimulates the vagal centers directly. It supports Straub's 3 suggestion that the slowing is due to a direct myocardial action, the sinus pacemaker becoming more responsive to vagal tone. In support of this viewpoint, Rothberger and Winterberg 4 have claimed that digitalis lowers the threshold to electrical stimulation of the vagus trunks, and Weger has observed 5 that it makes the parasympathetic endings in the intestine more irritable to stimulation by pilocarpine. However, Weiss 6 regards the slowing after digitalis as due to reflexes originating in the viscera innervated by the vagus. In order to obtain data regarding the validity of the first of these theories, we have attempted to demonstrate the presence or absence of an altered vagus sensitivity after digitalis, by comparing the responses in pulse rate to parasympathetic stimulants before and after administration of this drug.

The slowing caused by choline or acetyl choline in 6 anesthetized and unanesthetized dogs and cats, including one dog in which the adrenals were removed and the stellate ganglia and upper thoracic sympathetic trunks destroyed, was so slight that these drugs seemed of no value as tests for vagus sensitivity. We, therefore, selected physostigmine as a stimulant of the vagus endings. In 3 dogs, the vagi were cut aseptically, and after a 24-hour recovery period, 0.3 mg. per kilo of physostigmine was injected intravenously and the pulse rate changes recorded. The next day, 20 mg. digitalis per kilo, as the dilution of an active tincture, was given intravenously, and 2 hours later physostigmine was reinjected in the same dosage.