Iwasa A, Okumura K, Tabuchi T, Tsuchiya T, Tsunoda R, Matsunaga T, Tayama S, Yasue H
Division of Cardiology, Kumamoto University School of Medicine, Japan.
Eur J Pharmacol. 1998 Aug 28;356(1):31-40. doi: 10.1016/s0014-2999(98)00506-8.
The effects of pilsicainide on vagally induced atrial fibrillation and on electrophysiological parameters were compared with those of propafenone in alpha-chloralose-anesthetized dogs. Conduction velocity, effective refractory period, wavelength, averaged atrial fibrillation cycle length and activation sequence in the right atrial free wall were determined before and after drug administration. Pilsicainide (2 mg/kg/5 min and 3 mg/kg/h)(n=10) or propafenone (2 mg/kg/15 min and 4 mg/kg/h)(n=10) was intravenously infused during stable atrial fibrillation sustaining > 30 min. Pilsicainide terminated atrial fibrillation in nine dogs, while propafenone did so in three (p < 0.01). After the drug, conduction velocity was suppressed more in the pilsicainide than in the propafenone group(p < 0.01). There was no difference in effective refractory period after drug between the two groups. Mean wavelength was prolonged from 46.0 to 70.4 mm in the pilsicainide group and from 45.0 to 110.8 mm in the propafenone (p < 0.01 vs. pilsicainide). Activation mapping during atrial fibrillation showed Type II or III atrial fibrillation as previously defined [Konings, K.T.S., Kirchhof, C.J.H.J., Smeets, J.R.L.M., Wellens, H.J.J., Penn, O.C., Allessie, M.A., 1994. High-density mapping of electrically induced atrial fibrillation in humans. Circulation. Vol. 89, pp. 511-521.] before the drug, and changed to Type I before atrial fibrillation termination. Thus, pilsicainide was more effective to terminate vagally induced atrial fibrillation than was propafenone despite a greater effect of propafenone than of pilsicainide on wavelength. In this canine atrial fibrillation model, the suppression of conduction velocity may play an important role in changing the activation pattern of atrial fibrillation and thus, terminating atrial fibrillation.
在α-氯醛糖麻醉的犬中,比较了吡西卡尼与普罗帕酮对迷走神经诱发的心房颤动及电生理参数的影响。在给药前后,测定右心房游离壁的传导速度、有效不应期、波长、平均心房颤动周期长度及激动顺序。在持续超过30分钟的稳定心房颤动期间,静脉输注吡西卡尼(2mg/kg/5分钟和3mg/kg/小时)(n = 10)或普罗帕酮(2mg/kg/15分钟和4mg/kg/小时)(n = 10)。吡西卡尼使9只犬的心房颤动终止,而普罗帕酮使3只犬的心房颤动终止(p < 0.01)。给药后,吡西卡尼组的传导速度比普罗帕酮组受到更明显的抑制(p < 0.01)。两组给药后的有效不应期无差异。吡西卡尼组的平均波长从46.0mm延长至70.4mm,普罗帕酮组从45.0mm延长至110.8mm(与吡西卡尼相比,p < 0.01)。心房颤动期间的激动标测显示,给药前为先前定义的II型或III型心房颤动[Konings, K.T.S., Kirchhof, C.J.H.J., Smeets, J.R.L.M., Wellens, H.J.J., Penn, O.C., Allessie, M.A., 199年。人类电诱发心房颤动的高密度标测。循环。第89卷,第511 - 521页。],在心房颤动终止前转变为I型。因此,尽管普罗帕酮对波长的作用比吡西卡尼大,但吡西卡尼在终止迷走神经诱发的心房颤动方面比普罗帕酮更有效。在这个犬心房颤动模型中,传导速度的抑制可能在改变心房颤动的激动模式从而终止心房颤动方面起重要作用。