Abstract
With the A-V tissues subjected to a constant bombardment of impulses arising in the auricle by faradically maintained auricular fibrillation, the ventricular rate (of beats of supraventricular origin) was used as an indicator of A-V conductivity. Using this method, the following results were obtained on A-V conductivity: vagal stimulation produced a depression; sympathetic stimulation produced an enhancement; simultaneous or successive stimulation of the vagi and sympathetics was algebraically additive; acetylcholine and mecholyl produced a depression which was prevented by atropine and increased by eserine; adrenalin produced an enhancement; asphyxia produces a primary enhancement followed by a depression. These effects occurred in reverse order on recovery from asphyxia. The differences in direction, lag and persistence of the effects of vagus and sympathetic nerve stimulation were similar to the known differences in the action of these nerves on other cardiac properties. The resemblance of the effects on A-V conductivity between vagus stimulation and cholinergic drug action, and the resemblance between the effects of sympathetic stimulation and adrenalin, lent support to the view that the action of the nerves on A-V conductivity was mediated chemically.

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