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尼可地尔可抑制家兔体内由氯化铯诱导的早期后除极和室性心律失常。

Nicorandil suppresses early afterdepolarisation and ventricular arrhythmias induced by caesium chloride in rabbits in vivo.

作者信息

Takahashi N, Ito M, Saikawa T, Arita M

机构信息

Department of Laboratory Medicine, Medical College of Oita, Japan.

出版信息

Cardiovasc Res. 1991 Jun;25(6):445-52. doi: 10.1093/cvr/25.6.445.

Abstract

STUDY OBJECTIVE

Outward K current of cardiac membrane has been shown to be suppressed by caesium chloride (Cs) and enhanced by nicorandil, a coronary vasodilator. The aim of this study was to assess the effects of nicorandil on the Cs induced early afterdepolarisations and associated ventricular arrhythmias in the rabbit heart in vivo.

DESIGN

Intravenous bolus injections of Cs (1 mmol.kg-1) were given three times at 20 min intervals. Monophasic action potentials of the left ventricular endocardium and the ECG (lead II) were recorded simultaneously over 60 min, under the intrinsic (sinus node) cardiac rhythm.

EXPERIMENTAL MATERIAL

Eight rabbits were treated with Cs alone (control group); seven other rabbits were first treated with an intravenous infusion of nicorandil (0.2 mg.kg-1) (nicorandil treated group) and the effects of Cs were then examined.

MEASUREMENTS AND MAIN RESULTS

In the control group, Cs produced early afterdepolarisations, premature ventricular beats and ventricular tachycardias. The ventricular tachycardias included two different types: (1) non-sustained polymorphic ventricular tachycardia mimicking the torsade de pointes in patients with long QT syndrome; (2) sustained monomorphic ventricular tachycardia. In the nicorandil treated group, the amplitude of the early afterdepolarisations and the incidence of ventricular tachycardias were significantly less than in the control group.

CONCLUSIONS

Nicorandil suppresses the early afterdepolarisations and ventricular tachyarrhythmias induced by Cs, possibly by increasing the membrane K conductance.

摘要

研究目的

氯化铯(Cs)可抑制心脏细胞膜外向钾电流,而冠状动脉扩张剂尼可地尔可增强该电流。本研究旨在评估尼可地尔对家兔体内Cs诱导的早期后去极化及相关室性心律失常的影响。

设计

每隔20分钟静脉推注Cs(1 mmol·kg⁻¹),共三次。在心脏固有(窦房结)节律下,同步记录左心室内膜的单相动作电位和心电图(II导联)60分钟。

实验材料

8只家兔仅接受Cs治疗(对照组);另外7只家兔先静脉输注尼可地尔(0.2 mg·kg⁻¹)(尼可地尔治疗组),然后检测Cs的作用。

测量与主要结果

在对照组中,Cs产生早期后去极化、室性早搏和室性心动过速。室性心动过速包括两种不同类型:(1)类似于长QT综合征患者尖端扭转型室速的非持续性多形性室性心动过速;(2)持续性单形性室性心动过速。在尼可地尔治疗组中,早期后去极化的幅度和室性心动过速的发生率显著低于对照组。

结论

尼可地尔可能通过增加膜钾电导来抑制Cs诱导的早期后去极化和室性快速心律失常。

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