THE EFFECT OF DIGITALIS ON THE EXCITABILITY OF AUTONOMIC NERVES

¹ Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York

The decrease in sinus rate in response to electrical stimulation of the vagus is enhanced by digitalis. The mechanism is undefined. Available evidence does not permit the site or sites of action to be restricted to the nerve, the autonomic ganglia, the nerve terminals or the postjunctional membrane and cholinergic receptor. Experiments were performed on cats, anesthetized with pentobarbital or chloralose-urethane, to demonstrate the effects of systemic administration of ouabain on the excitability of autonomic nerves. The decentralized preganghionic and postganglionic cervical sympathetic nerve trunks were stimulated with submaximal trains of pulses at 1 and 10 cps, and the evoked action potentials were recorded from both the pre- and postganglionic sympathetic nerve trunks. Also, during stimulation of the decentralized cervical vagus trunk, the evoked action potentials were recorded from the vagal branch coursing into the sinus node region. Under control conditions the size of the evoked action potentials increased with increasing stimulus frequency and train duration. After an infusion of ouabain (0.04-0.09 mg/kg i.v.), the maximal change in size of the evoked action potentials occurred at lower stimulus frequency, occurred earlier in the course of a train of stimuli and usually was greater in magnitude. Indirect evidence sug gesting that the same events occur in the postganglionic sympathetic nerve trunk also was obtained. In the sinus branch of the vagus, the same dose of ouabain enhanced the size of the evoked action potentials, increased the interval between the stimulus and the onset of the evoked action potentials and increased the excitability of several fiber groups. These data indicate that ouabain changes the number of fibers responding to a constant strength stimulus and may enhance the effect of the vagus on sinus rate in part through an action which increases nerve excitability.