Abstract
The perfusion of the AV node artery in eight dogs in situ was performed under constant pressure of 100mm Hg. Ganglionic stimulating agents, i.e., nicotine, DMPP and McN-A-343 were administered into the AV node artery. Doses above 3μg of nicotine always induced complete AV block. DMPP induced also complete AV block, but frequently followed by nodal tachycardia. These AV blocks were completely prevented by atropine or tetrodotoxin, and nodal tachycardia was blocked by propranolol. On the contrary, McN-A-343 at doses from 10μg to 1mg had entirely no effect on the AV conduction.
The authors conclude that the complete AV block induced by nicotine or DMPP is due to the stimulation of parasympathetic ganglia and that nodal tachycardia following initial AV block induced by DMPP is due to catecholamine release from sympathetic nerve endings and not by stimulation of sympathetic ganglia, because McN-A-343 causes neither AV block nor nodal tachycardia.
