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小鼠体内心脏电生理学研究。

In vivo cardiac electrophysiology studies in the mouse.

作者信息

Berul C I, Aronovitz M J, Wang P J, Mendelsohn M E

机构信息

Division of Pediatric Cardiology, New England Medical Center, Boston, MA 02111, USA.

出版信息

Circulation. 1996 Nov 15;94(10):2641-8. doi: 10.1161/01.cir.94.10.2641.

Abstract

BACKGROUND

This report describes a novel in vivo mouse epicardial cardiac electrophysiology study based on clinical protocols used to evaluate cardiac conduction in human patients. The technique allows extensive electrophysiological evaluation, including the response to pacing, programmed stimulation, and pharmacological agents.

METHODS AND RESULTS

Surface six-lead ECG data from 18 C57BL/6J mice are presented. Normal cardiac conduction properties for 14 of 18 mice that underwent the procedure are summarized, including determination of sinus node recovery times, AV conduction properties, and atrial, AV, and ventricular effective refractory periods. A subset of six mice was studied after the administration of either procainamide (n = 3) or quinidine (n = 3). All animals in the procainamide group developed either second-degree or complete AV block spontaneously. The sinus cycle length and refractory periods prolonged on procainamide or quinidine, but no tachyarrhythmias could be induced with atrial or ventricular programmed stimulation.

CONCLUSIONS

This mouse electrophysiology method allows rapid assessment of the conduction properties of the murine heart. The ability to analyze cardiac conduction in normal and transgenic mice provides a powerful tool for examining molecular electrophysiological mechanisms in normal physiology and disease states.

摘要

背景

本报告描述了一项基于用于评估人类患者心脏传导的临床方案的新型体内小鼠心外膜心脏电生理学研究。该技术允许进行广泛的电生理评估,包括对起搏、程控刺激和药物的反应。

方法和结果

展示了18只C57BL/6J小鼠的六导联体表心电图数据。总结了接受该手术的18只小鼠中14只的正常心脏传导特性,包括窦房结恢复时间、房室传导特性以及心房、房室和心室有效不应期的测定。对6只小鼠的一个亚组在给予普鲁卡因胺(n = 3)或奎尼丁(n = 3)后进行了研究。普鲁卡因胺组的所有动物均自发出现二度或完全性房室传导阻滞。使用普鲁卡因胺或奎尼丁后,窦性周期长度和不应期延长,但心房或心室程控刺激未诱发快速性心律失常。

结论

这种小鼠电生理学方法能够快速评估小鼠心脏的传导特性。在正常和转基因小鼠中分析心脏传导的能力为研究正常生理和疾病状态下的分子电生理机制提供了一个强大的工具。

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