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《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:

2002年第6期

页码:

477-479

栏目:

实验研究

出版日期:

2002-11-01

文章信息/Info

Title:

Effects of propafenone on transmembrane action potential,effective refractory period and ventricular fibrillation threshold of ischemic myocardium in vivo rabbits

作者:

黄国明¹;  李庚山²;  周秋凤²;  乔怀宇¹

1.解放军第九四医院心内科,江西南昌330002; 2.武汉大学第一临床学院心内科

Author(s):

HUANG Guo-ming¹; LI Geng-shan²;  ZHOU Qiu-feng²;  QIAO Huai-yu¹

1. Department of Cardiology, 94th hospital of PLA, Nanchang, Jiangxi 330002, China; 2. Department of Cardiology, First Clinical College of Wuhan Univesity

关键词:

普罗帕酮; 心肌缺血; 跨膜动作电位; 有效不应期; 室颤阈

Keywords:

propafenone;  myocardial ischemia;  transmembrone action potential;  effective refractory period;  ventricular fibrillation threshold

分类号:

-

DOI:

-

文献标识码:

A

摘要:

目的 观察普罗帕酮(PF)对在体家兔急性缺血心肌细胞跨膜动作电位(TAP)、有效不应期(ERP)、舒张期阈电位(DTP)和室颤阈(VFT)的影响,探讨其抗缺血性心律失常的机制。方法 开胸结扎兔冠状动脉左前降支,用玻璃微电极记录静脉注射PF(实验组)或葡萄糖(对照组)前、后缺血区心外膜下心肌细胞的TAP;通过程控刺激测量缺血区DTP,ERP;用两倍阈电位的脉冲刺激右室心肌,并以5~10 V递增,检测VFT。结果 PF明显降低缺血心肌细胞TAP 0相最大上升速度(Vmax)和振幅(均P<0.01),延长复极90%时的动作电位时程(APD90)(P<0.01),但对静息电位无明显影响;PF显著提高缺血心肌的DTP和VFT(均P<0.01),延长ERP(P<0.01)。结论 PF进一步降低Vmax、延长APD和ERP,使单向阻滞转为双向阻滞而终止折返,这可能是PF抗缺血性心律失常的主要电生理机制。

Abstract:

AIM To discuss the antiarrhythmic mechanism of propafenone (PF) by investigating the effects of PF on transmembrane action potential (TAP), effective refractory period (ERP), diastolic threshold potential (DTP), and ventricular fibrillation threshold (VFT) of ischemic myocardiumin vivorabbits.METHODS: After ligation of left anterior descending artery, TAPs of ischemic sites were recorded with glass microelectrode before and 10 min after injection of PF or glucose; DTP and ERP were measured using a programmable stimulator; right ventricular stimuli were introduced at twice diastolic threshold and subsequently increased in 5~10 V intervals to measure VFT.RESULTS: PF apparently decreased the maximum upstroke velocity (Vmax) and amplitude of TAP and prolonged action potential duration at 90% of repolarization (allP<0.01) without affecting resting potential; PF significantly enhanced DTP and VFT of ischemic myocardium and increased ERP (allP<0.01).CONCLUSION: Further depressing of Vmaxand prolonging of APD and ERP converse unidirectional block into bidirectional block, which may be the main mechanism of antiarrhythmia of PF in ischemic heart disease.

参考文献/References

[1] Faber TS, Zehender M, Krahnefeld O,et al. Propafenone during acute myocardial ischemia in patients: a double-blind, randomized, placebo-controlled study [J].J Am Coll Cardiol,1997, 29(3): 561-567.

[2] Mastropasqua F, Totaro P, Massari F,et al. Double-blind randomized placebo-controlled study of the effects of slow release and immediate release forms of propafenone in patients ventricular extrasystole symptoms[J].Cardiologia, 1998, 43(6): 617 -623.

[3] Koller B, Franz MR. New classification of moricizine and propafenone based on electrophysiologic and electrocardiographic data from isolated rabbit heart [J].J Cardiovasc Pharmacol, 1994, 24(5): 753-760.

[4] Takahashi N, Ito M, Ishida S,et al. Electrophysiological effects of SD-3212, a novel antiarrhythmic agent, on rabbit hearts in vivoandin vitro[J].J Cardiovasc Pharmacol, 1995, 25(6): 1006-1011.

[5] Yin H, Sherif N, Caref EB,et al. Actions of lidocaine on reentrant ventricular rhythms in the subacute myocardial infarction period in dogs[J].Am J Physiol, 1997, 272(1 Pt 2): H299-H300.

[6] Bardou AL, Auger PM, Achour S,et al. Effect of myocardial infarction and ischemia on induction of cardiac reentries and ventricular fibrillation[J].Acta Biotheor, 1995,43(4): 363-372.

备注/Memo

备注/Memo:

收稿日期：2001-10-15.

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更新日期/Last Update: 2002-11-01