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小鼠心肌梗死后的自发性和诱发性室性心律失常。

Spontaneous and inducible ventricular arrhythmias after myocardial infarction in mice.

作者信息

Betsuyaku Tetsuo, Kanno Shigeto, Lerner Deborah L, Schuessler Richard B, Saffitz Jeffrey E, Yamada Kathryn A

机构信息

Department of Medicine (Cardiovascular Division), Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

Cardiovasc Pathol. 2004 May-Jun;13(3):156-64. doi: 10.1016/S1054-8807(03)00152-2.

Abstract

INTRODUCTION

Remodeling of gap junctions has been implicated in development of ventricular arrhythmias following myocardial infarction (MI) but the specific contribution of reduced electrical coupling is not known. We addressed this question using hearts from mice heterozygous for a connexin43 null allele (Cx43(+/-)).

METHODS

To determine whether Cx43-deficient mice exhibit increased spontaneous ventricular arrhythmias in the setting of chronic ischemic heart disease, radiofrequency transmitters were implanted in wild-type and Cx43(+/-) mice 2 days or 9 weeks after left anterior descending coronary artery ligation or sham operations. ECGs were recorded from unanesthetized, unrestrained mice 1 and 10 weeks after MI. Isolated, perfused hearts excised 1 and 10 weeks after MI were subjected to programmed electrical stimulation to induce arrhythmias.

RESULTS AND CONCLUSIONS

Hearts with infarcts exhibited more spontaneous and inducible arrhythmias, but there was no significant difference between wild-type and Cx43-deficient mice. Fewer hearts exhibited spontaneous ventricular tachycardia (VT) in vivo than were inducible in vitro, suggesting that structural and functional substrates for inducible VT in isolated hearts may not be sufficient for initiation and maintenance of sustained VT in vivo. Previous studies have shown that Cx43-deficient mice exhibit more VT than wild-type mice during acute regional ischemia. Mice with MI exhibit increased arrhythmias. However, reduced coupling in Cx43-deficient mice does not significantly enhance spontaneous or inducible VT after MI.

摘要

引言

间隙连接重塑与心肌梗死(MI)后室性心律失常的发生有关,但电偶联减少的具体作用尚不清楚。我们使用连接蛋白43无效等位基因杂合子(Cx43(+/-))小鼠的心脏来解决这个问题。

方法

为了确定Cx43缺陷小鼠在慢性缺血性心脏病情况下是否表现出自发性室性心律失常增加,在左冠状动脉前降支结扎或假手术后2天或9周,将射频发射器植入野生型和Cx43(+/-)小鼠体内。在心肌梗死后1周和10周,从未麻醉、不受约束的小鼠记录心电图。在心肌梗死后1周和10周切除的离体灌注心脏接受程序性电刺激以诱发心律失常。

结果与结论

有梗死的心脏表现出更多的自发性和诱发性心律失常,但野生型和Cx43缺陷小鼠之间没有显著差异。体内表现出自发性室性心动过速(VT)的心脏比体外可诱导的心脏少,这表明离体心脏中可诱导VT的结构和功能底物可能不足以在体内启动和维持持续性VT。先前的研究表明,在急性局部缺血期间,Cx43缺陷小鼠比野生型小鼠表现出更多的VT。患有心肌梗死的小鼠心律失常增加。然而,Cx43缺陷小鼠中偶联减少并没有显著增强心肌梗死后的自发性或诱发性VT。

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