Pathobiology of ischaemic stroke: an integrated view

被引：3136

作者：

Dirnagl, U ^{[1
]}

Iadecola, C

Moskowitz, MA

机构：

[1] Charite Hosp, Dept Neurol, D-10098 Berlin, Germany

[2] Univ Minnesota, Sch Med, Lab Cerebrovasc Biol & Stroke, Dept Neurol, Minneapolis, MN 55455 USA

[3] Harvard Univ, Sch Med, Stroke Res Lab, Massachusetts Gen Hosp, Charlestown, MA 02129 USA

[4] Harvard Univ, Sch Med, Neurosurg Serv, Massachusetts Gen Hosp, Charlestown, MA 02129 USA

[5] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Charlestown, MA 02129 USA

[6] Massachusetts Gen Hosp, Charlestown, MA 02129 USA

来源：

TRENDS IN NEUROSCIENCES | 1999年 / 22卷 / 09期

关键词：

D O I：

10.1016/S0166-2236(99)01401-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from a complex series of pathophysiological events that evolve in time and space. In this article, the relevance of excitotoxicity, peri-infarct depolarizations, inflammation and apoptosis to delayed mechanisms of damage within the peri-infarct zone or ischaemic penumbra are discussed. While focusing on potentially new avenues of treatment, the issue of why many clinical stroke trials have so far proved disappointing is addressed. This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.

引用

页码：391 / 397

页数：7

共 86 条

[1] The Bcl-2 protein family: Arbiters of cell survival [J].