ABSTRACT
An inflammatory reaction has been demonstrated in the brain following ischemia reperfusion (Kochanek et al., 1992; Ember et al., 1994). Inflammation is a consequence of activation and interactions of major inflammatory cells including macrophages, neutrophils, endothelial cells, and platelets. The major inflammatory mediators are cytokines, eicosanoids, kinins, and proteases. Expression of pro-inflammatory cytokines (Liu et al., 1993a; Siren et al., 1993) and increased accumulation of eicosanoids and kinins (Hsu et al., 1988) have been noted following cerebral ischemiareperfusion. Reactive oxygen species (ROS) are free radicals that have been implied in the pathogenesis of tissue damage in disease states. ROS are also major inflammatory mediators which are generated by inflammatory cells via arachidonic acid, nitric oxide, or xanthine oxidase cascade or lipid peroxidation.
