A study of the verapamil-induced changes in conductivity and refractoriness and monophasic action potentials of the dog heart in situ.
In the dog heart in situ, verapamil 0.30 mg/kg injected intravenously did not impair intraatrial, His--Purkinje and intraventricular conduction. The monophasic action potential (MAP) derived from the right atrium and ventricle was not altered by the drug. The functional refractory period (FRP) and the effective refractory period (ERP) of the atrium was not changed by verapamil. However, the drug caused a small but statistically significant decrease in the ratio between 50 and 90% repolarization, respectively, and the ERP of the right atrium, i.e. the ERP of the atrium increased in relation to the MAP duration. Verapamil used a marked reduction of the conduction velocity within and a pronounced increase of the AV nodal FRP and ERP. These changes were reversed by a rapid injection of calcium gluconate 40 mg/kg. The sinus node automaticity was not influenced by verapamil.
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects; D002036:Bundle of His / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology; D004285:Dogs; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects*; D008297:Male; D008954:Models, Biological; D011690:Purkinje Fibers / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology*
D014700:Verapamil; D002118:Calcium