Free radical scavengers and spin traps--therapeutic implications for ischemic stroke

Abstract

Ischemic stroke comprises a complex cascade of pathophysiological mediators among which reactive oxygen species (ROS) play a pivotal role. Although oxidative stress as one major component contributing to ischemia-reperfusion injury has been thoroughly studied before, efficient treatment options for patients with ischemic stroke have so far not been transferred into clinical practice. In this review, the authors first describe some of the fundamental pathophysiological mechanisms that are involved in ROS generation after cerebral ischemia. Thereafter, antioxidant defense mechanisms and pharmacological manipulation of oxidative stress in various models of experimental cerebral ischemia are reviewed. The authors finally comment on recent clinical studies analyzing the effect of an antioxidative therapy after ischemic stroke and present a short outlook for further studies on ROS-mediated injury after stroke.