Effects on atrio-ventricular conduction of alinidine and falipamil injected into the AV node artery of the anesthetized dog.

The effects of the bradycardic agents alinidine and falipamil, on atrio-ventricular (AV) conduction were compared with those of other negative chronotropic agents, acetylcholine (ACh), carbachol (CCh), adenosine and verapamil, in open-chest, anesthetized dogs. When each drug was selectively administered into the AV node artery, none of them changed the sinus rate and arterial blood pressure. Although alinidine did not significantly change the atrio-ventricular conduction time (AVCT), falipamil and others induced a dose-dependent prolongation of the AVCT. The order of the AVCT prolongation was CCh greater than ACh greater than verapamil much greater than adenosine greater than falipamil much greater than alinidine. ACh, CCh and verapamil frequently caused second or third degree AV block at higher doses. The His bundle electrocardiogram revealed that all AV blocks occurred between the atrium and the His bundle (A-H block). The CCh-induced prolongation of the AVCT, but not the adenosine-induced prolongation, was significantly suppressed by treatment with alinidine or falipamil. These results indicate that alinidine scarcely affects AV conduction in the in situ dog heart and that the muscarinic cholinergic receptor blocking effect of alinidine or falipamil modifies the AVCT secondarily when vagal activity is maintained.