Reduction of reperfusion-induced ventricular fibrillation and infarct size via heme oxygenase-1 overexpression in isolated mouse hearts

被引：13

作者：

Bak, Istvan ^{[1
]}

Czompa, Attila ^{[1
]}

Juhasz, Bela ^{[1
]}

Lekli, Istvan ^{[1
]}

Tosaki, Arpad ^{[1
]}

机构：

[1] Univ Debrecen, Dept Pharmacol, Hlth Sci Ctr, Fac Pharm, H-4012 Debrecen, Hungary

来源：

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | 2010年 / 14卷 / 09期

关键词：

ischemia; reperfusion; isolated mouse hearts; HO-1; transgenic; knockout; CARBON-MONOXIDE; MYOCARDIUM; ARRHYTHMIA; GENE;

D O I：

10.1111/j.1582-4934.2010.01142.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Heme oxygenase-1 (HO-1), also known as heat shock protein 32 (hsp-32) is a stress-induced cytoprotective protein. The present investigation evaluated the capacity of HO-1 to reduce the incidence of reperfusion-induced ventricular fibrillation (VF) and infarct size. HO-1 transgenic (Tg) mice were generated using a rat HO-1 genomic transgene. Isolated mouse hearts obtained from Tg and non-transgenic (NTg) groups were exposed to 20 min. of global ischemia and 120 min. of reperfusion. Epicardial electrocardiogram was recorded to monitor the incidence of reperfusion-induced VF and at the end of the reperfusion period, detection of HO-1 by immunohistochemistry and measurement of infarct size using the tetrazolium chloride method were carried out. Results shown here provide additional support for cardioprotective effects of HO-1 as demonstrated by the reduced infarct size. Moreover, overexpression of the HO-1 efficiently reduced the incidence of ischemia/reperfusion induced VF in HO-1 Tg mice.

引用

页码：2268 / 2272

页数：5

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