The influence of nicotine in modulating vulnerability to atrial tachycardia and fibrillation (AT/AF) remains ill defined. The isolated hearts of six young (2-3 mo) and six old (22-24 mo) male Fischer 344 rats were Langendorff perfused at 5 ml/min with oxygenated Tyrode solution at 37°C, and the whole heart was also superfused with warmed oxygenated Tyrode solution at 15 ml/min. Nicotine prolonged the interatrial conduction time and effective refractory period that were significantly (P < 0.05) higher in the old than in the young rats in a concentration-dependent manner. Nicotine had a biphasic effect on burst atrial pacing-induced AT in both groups, increasing it at 10-30 ng/ml while decreasing it at 50-100 ng/ml (P < 0.01). Nicotine at 10-100 ng/ml increased burst atrial pacing-induced AF in the young rats but suppressed it in the old rats (P < 0.01). Optical mapping showed the presence of multiple independent wavefronts during AF and a single periodic large wavefront during AT in both groups. Nicotine, at concentrations found in the blood of smokers (30-85 ng/ml), exerts biphasic effects on inducible AT/AF in young rats and suppresses it in the old rats by causing high degrees of interatrial conduction block.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 54-5|
|State||Published - 1 Nov 2003|
- Refractory period