Nitric oxide and cerebral ischernic preconditioning

被引：72

作者：

Huang, PL

机构：

[1] Harvard Univ, Sch Med, Div Cardiol, Charlestown, MA 02129 USA

[2] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA

来源：

CELL CALCIUM | 2004年 / 36卷 / 3-4期

关键词：

nitric oxide; cerebral ischemia; preconditioning;

D O I：

10.1016/j.ceca.2004.02.007

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Nitric oxide (NO) is an important mediator of cerebral blood flow and metabolism. As a vasodilator, NO regulates cerebral blood flow, and couples regional brain perfusion with metabolic activity. Following cerebral ischemia, NO levels rise significantly due to activation of neuronal nitric oxide synthase by NMDA receptor mediated calcium entry. Depending on its tissue and enzymatic source, NO may be protective or toxic. This article reviews the effects of NO following cerebral ischemia, the signaling pathways through which NO acts, and its potential roles in cerebral ischemic preconditioning, (C) 2004 Elsevier Ltd. All rights reserved.

引用

页码：323 / 329

页数：7

共 56 条

[1] Nitric oxide synthases: structure, function and inhibition [J].