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心肌梗死与一氧化氮

Myocardial infarction and nitric oxide.

作者信息

Bing R J, Suzuki H

机构信息

Department of Experimental Cardiology, Huntington Medical Research Institutes, Pasadena, CA 91101, USA.

出版信息

Mol Cell Biochem. 1996 Jul-Aug;160-161:303-6. doi: 10.1007/BF00240063.

Abstract

The report deals with the induction of the inducible form of nitric oxide synthase (iNOS) in infarcted heart muscle of rabbit and man. In the rabbit, nitric oxide synthase was significantly increased in the infarcted area beginning on the third day following ligation of a coronary artery. iNOS induction occurred primarily in macrophages. In man, iNOS immunoreactivity was also primarily localized in macrophages on the seventh day following death from myocardial infarction. Of the specific inhibitors of iNOS in infarcted heart muscle, S-methylisothiourea (SMT) was the most potent. Its greatest effect occurred in the normal non-affected area of the heart. Dexamethasone and cyclosporin A failed to inhibit iNOS. Apoptosis of macrophages commenced two days following ligation of a coronary artery.

摘要

该报告探讨了兔和人梗死心肌中诱导型一氧化氮合酶(iNOS)的诱导情况。在兔中,冠状动脉结扎后第三天开始,梗死区域的一氧化氮合酶显著增加。iNOS的诱导主要发生在巨噬细胞中。在人身上,心肌梗死后第七天,iNOS免疫反应性也主要定位于巨噬细胞。在梗死心肌中iNOS的特异性抑制剂中,S-甲基异硫脲(SMT)最为有效。其最大作用发生在心脏正常未受影响的区域。地塞米松和环孢素A未能抑制iNOS。冠状动脉结扎两天后巨噬细胞开始凋亡。

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