Kojima Jisho, Niwano Shinichi, Moriguchi Masahiko, Ikeda Kazuko, Inuo Kimiatsu, Saito Junko, Izumi Toru
Department of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
Circ J. 2003 Apr;67(4):340-6. doi: 10.1253/circj.67.340.
The heterogeneous process of atrial electrical remodeling (AER) in the canine rapid atrial stimulation model has been previously reported although it has been reported that a sodium channel blocker might suppress the shortening of the atrial effective refractory period (AERP), its effect on long-term electrical remodeling is unknown. In the present study, the effect of pilsicainide on AER was evaluated. The right atrial appendage (RAA) was paced at 400 beats/min for 2 weeks. In the RAA, Bachmann's bundle (BB), the right atrium near the inferior vena cava (IVC) and in the left atrium (LA), AERP, AERP dispersion (AERPd) and the inducibility of atrial fibrillation (AF) were evaluated at several time points of the pacing phase and the recovery phase (1 week). The same protocol was performed during the administration of pilsicainide (4.5 mg/kg per day) and the parameters were compared with the controls. In the control dogs, the AERP was significantly shortened by rapid pacing at all atrial sites studied and the AERP shortening (DeltaAERP) was larger at the RAA and LA sites (p<0.03). However, pilsicainide decreased these DeltaAERPs at all 4 atrial sites. AERPd was increased during the pacing phase whereas it was decreased during the recovery phase in the control dogs. In contrast, this pacing-induced AERPd was attenuated by the administration of pilsicainide. The AF inducibility was highest at the LA site in both groups, and the inducibility was lower in the pilsicainide group than the control group at all atrial sites. During the rapid pacing phase, the ventricular heart rate was significantly lower in the pilsicainide group than the control because of intra-atrial conduction block. In a canine rapid right atrial stimulation model, pilsicainide suppressed the shortening of the AERP at all atrial sites, possibly through the improvement of the hemodynamics as well as the action of the Na - Ca exchanger.
尽管先前已有报道犬快速心房刺激模型中存在心房电重构（AER）的异质性过程，并且有报道称钠通道阻滞剂可能会抑制心房有效不应期（AERP）的缩短，但其对长期电重构的影响尚不清楚。在本研究中，评估了吡西卡尼对AER的影响。右心耳（RAA）以400次/分钟的频率起搏2周。在RAA、巴赫曼束（BB）、下腔静脉（IVC）附近的右心房以及左心房（LA），在起搏期和恢复阶段（1周）的几个时间点评估AERP、AERP离散度（AERPd）和房颤（AF）的诱导率。在给予吡西卡尼（每天4.5mg/kg）期间执行相同的方案，并将参数与对照组进行比较。在对照犬中，在所研究的所有心房部位，快速起搏均使AERP显著缩短，且RAA和LA部位的AERP缩短（ΔAERP）更大（p<0.03）。然而，吡西卡尼在所有4个心房部位均降低了这些ΔAERP。在对照犬中，起搏期AERPd增加，而恢复期则降低。相比之下，吡西卡尼的给药减弱了这种起搏诱导的AERPd。两组中LA部位的AF诱导率最高，且在所有心房部位，吡西卡尼组的诱导率均低于对照组。在快速起搏期，由于心房内传导阻滞，吡西卡尼组的心室心率显著低于对照组。在犬快速右心房刺激模型中，吡西卡尼可能通过改善血流动力学以及钠-钙交换体的作用，抑制了所有心房部位AERP的缩短。
