2010年5月
Effect of Bepridil in Atrial Fibrillation Inducibility Facilitated by Vagal Nerve Stimulation - Prevention of Vagal Nerve Activation-Induced Shortening of the Atrial Action Potential Duration
CIRCULATION JOURNAL
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- 巻
- 74
- 号
- 5
- 開始ページ
- 895
- 終了ページ
- 902
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1253/circj.CJ-09-0716
- 出版者・発行元
- JAPANESE CIRCULATION SOC
Background: Because bepridil blocks multiple myocardial ionic channels, including the muscarinic acetylcholine receptor-operated potassium current (I(KAch)), bepridil is expected to suppress atrial fibrillation (AF) mediated by vagal nerve stimulation (VNS).
Methods and Results: The therapeutic effects of bepridil were studied with a special focus on heart rate variability (HRV) in a canine model of AF. During VNS, AF was induced in 9 of 9 experiments before, vs 3 of 9 experiments after administration of bepridil (P<0.01). During 350 ms atrial pacing, VNS shortened the right and left atrial monophasic action potentials at 90% repolarization (MAP90) by -31 +/- 8% and -22 +/- 12%, respectively, vs -10 +/- 13% and -6 +/- 8%, respectively, after bepridil (P<0.01, N=9). Bepridil prolonged the sinus cycle length, although it had no significant effect on the conduction time measured at 300 ms pacing. Statistically insignificant change was observed in the VNS-induced slowing of the sinus cycle length and in the VNS-induced increase in high frequency amplitude of HRV before (1.2 +/- 0.7 to 5.3 +/- 4.0 ms) vs after (1.7 +/- 0.8 to 5.4 +/- 2.3 ms) bepridil administration.
Conclusions: Bepridil prevented the VNS-induced shortening of atrial MAP90 and suppressed the inducibility of AF during VNS in two-thirds of the experiments. As far as this study shows, it may be possible that inhibition of I(KAch) played a part in this antifibrillatory effect. (Circ J 2010; 74: 895-902)
Methods and Results: The therapeutic effects of bepridil were studied with a special focus on heart rate variability (HRV) in a canine model of AF. During VNS, AF was induced in 9 of 9 experiments before, vs 3 of 9 experiments after administration of bepridil (P<0.01). During 350 ms atrial pacing, VNS shortened the right and left atrial monophasic action potentials at 90% repolarization (MAP90) by -31 +/- 8% and -22 +/- 12%, respectively, vs -10 +/- 13% and -6 +/- 8%, respectively, after bepridil (P<0.01, N=9). Bepridil prolonged the sinus cycle length, although it had no significant effect on the conduction time measured at 300 ms pacing. Statistically insignificant change was observed in the VNS-induced slowing of the sinus cycle length and in the VNS-induced increase in high frequency amplitude of HRV before (1.2 +/- 0.7 to 5.3 +/- 4.0 ms) vs after (1.7 +/- 0.8 to 5.4 +/- 2.3 ms) bepridil administration.
Conclusions: Bepridil prevented the VNS-induced shortening of atrial MAP90 and suppressed the inducibility of AF during VNS in two-thirds of the experiments. As far as this study shows, it may be possible that inhibition of I(KAch) played a part in this antifibrillatory effect. (Circ J 2010; 74: 895-902)
- リンク情報
- ID情報
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- DOI : 10.1253/circj.CJ-09-0716
- ISSN : 1346-9843
- PubMed ID : 20379003
- Web of Science ID : WOS:000277226100016