Cerebral ischemia and inflammation. Review uri icon

Overview

abstract

  • Cerebral ischemia is accompanied by a marked inflammatory reaction that is initiated by ischemia-induced expression of cytokines, adhesion molecules, and other inflammatory mediators, including prostanoids and nitric oxide. Preclinical studies suggest that interventions that are aimed at attenuating such inflammation reduce the progression of brain damage that occurs during the late stages of cerebral ischemia. In particular, strategies that block the activity of inflammation-related enzymes, such as inducible nitric oxide synthase and cyclo-oxygenase-2, reduce ischemic damage with an extended therapeutic window. Although a clinical trial using murine antibodies against intercellular adhesion molecule-1 did not show benefit in patients with ischemic stroke, recent data indicate that immune activation induced by the heterologous protein may have played an important role in the failure of this trial. Therefore, there is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late stages of cerebral ischemia.

publication date

  • February 1, 2001

Research

keywords

  • Brain Ischemia
  • Encephalitis

Identity

Scopus Document Identifier

  • 0035143182

Digital Object Identifier (DOI)

  • 10.1097/00019052-200102000-00014

PubMed ID

  • 11176223

Additional Document Info

volume

  • 14

issue

  • 1