Rate-dependent effects of ajmaline and propafenone on atrioventricular conduction

• Published in: European journal of pharmacology 1996-08, Vol.310 (1), p.29-35
• Main Authors: Stark, Gerhard, Schwarzl, Ingrid, Stark, Ulrike, Decrinis, Martin, Tritthart, Helmut A.
• Format: Article
• Language: English
• Subjects: Ajmaline; Ajmaline - pharmacology; Animals; Anti-Arrhythmia Agents - pharmacology; Antiarythmic agents; Atrioventricular Node - drug effects; Atrioventricular Node - physiology; AV-node; Biological and medical sciences; Cardiovascular system; Electrocardiography; Female; Guinea Pigs; Heart - physiology; Heart Conduction System - drug effects; Male; Medical sciences; Perfusion; Pharmacology. Drug treatments; Propafenone; Propafenone - pharmacology; Rate dependence; Time constant
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/0014-2999(96)00378-0

The aim of the present study was to characterize the time dependence of the depressant effects of ajmaline and propafenone on the Ca 2+-channel-dependent tissue of the atrioventricular node in isolated guinea pig hearts perfused by the method of Langendorff. Ajmaline at a concentration of 0.03 μM and propafenone at a concentration of 0.3 μM caused a significant and comparable prolongation of the His bundle and atrioventricular conduction time (AVCT). When the pacing cycle length was abruptly shortened from 240 to 180 ms, the mean time constant ( τ on) of the rate-dependent AVCT prolongation was comparable for ajmaline and propafenone. In contrast, if the pacing cycle length was abruptly increased from 180 to 240 ms the mean time constant ( τ off) for ajmaline was significantly higher than for propafenone. The rate-dependent increase of the atrioventricular effective refractory period was significantly more pronounced in the presence of ajmaline than of propafenone. Ajmaline and propafenone affect the Ca 2+-channel-dependent tissue of the myocardium. The more pronounced rate-dependent effect of ajmaline on the atrioventricular effective refractory period may be explained by a slower dissociation kinetic from the channel.