Chiba Toshiki, Kondo Naoto, Takahara Akira
Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Toho University, 2-2-1 Miyama, Funabashi, Chiba 274-8510, Japan; Department of R&D, Fukushima Research Laboratories, TOA EIYO Ltd., Iizaka, Fukushima 960-0211, Japan.
Department of R&D, Fukushima Research Laboratories, TOA EIYO Ltd., Iizaka, Fukushima 960-0211, Japan.
J Pharmacol Sci. 2016 Mar;130(3):170-6. doi: 10.1016/j.jphs.2016.02.007. Epub 2016 Mar 2.
Electrical remodeling plays a pivotal role in maintaining the reentry during atrial fibrillation. In this study, we assessed influence of electrical remodeling on pharmacological manipulation of the atrial refractoriness in rabbits. We used an atrial electrical remodeling model of the rabbit, subjected to rapid atrial pacing (RAP; 600 beats/min) for 2-4 weeks, leading to shortening of atrial effective refractory period (AERP). Intravenous administration of dl-sotalol (6 mg/kg), bepridil (1 mg/kg), amiodarone (10 mg/kg) or vernakalant (3 mg/kg) significantly prolonged the AERP both in the control and RAP rabbits. The extents in the RAP rabbits were similar to those in the control animals. On the other hand, prolonging effects of intravenously administered ranolazine (10 mg/kg) or tertiapin-Q (0.03 mg/kg) on the AERP in the RAP rabbits were more potent than those in the control animals. These results suggest that rapid pacing-induced electrical remodeling effectively modified the prolonging effects of ranolazine and tertiapin-Q on the AERP in contrast to those of clinically available antiarrhythmic drugs, dl-sotalol, bepridil amiodarone and vernakalant.
电重构在维持房颤期间的折返中起关键作用。在本研究中,我们评估了电重构对兔心房不应期药物调控的影响。我们使用兔心房电重构模型,对其进行快速心房起搏(RAP;600次/分钟)2 - 4周,导致心房有效不应期(AERP)缩短。静脉注射dl - 索他洛尔(6mg/kg)、苄普地尔(1mg/kg)、胺碘酮(10mg/kg)或维纳卡兰(3mg/kg)在对照组和RAP兔中均显著延长AERP。RAP兔中的延长程度与对照动物相似。另一方面,静脉注射雷诺嗪(10mg/kg)或替地品 - Q(0.03mg/kg)对RAP兔AERP的延长作用比对照动物更强。这些结果表明,与临床可用的抗心律失常药物dl - 索他洛尔、苄普地尔、胺碘酮和维纳卡兰相比,快速起搏诱导的电重构有效地改变了雷诺嗪和替地品 - Q对AERP的延长作用。