Cerebral ischemia and inflammation

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. P reclinical studies suggest that interventions that are aimed at attenuating such inflammation reduce the progression of brain damage that occurs durin g the late stages of cerebral ischemia. In particular, strategies that bloc k the activity of inflammation-related enzymes, such as inducible nitric ox ide synthase and cyclooxygenase-2, reduce ischemic damage with an extended therapeutic window. Although a clinical trial using murine antibodies again st 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 t his trial. Therefore, there is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late s tages of cerebral ischemia, Curr Opin Neurol 14:89-94. (C). 2001 Lippincott Williams & Wilkins.