Detection of hydroxyl radicals in rat striatum during transient focal cerebral ischemia: possible implication in tissue damage.

As increasing arguments suggest that the reperfusion phase following an ischemic insult may aggravate tissue injury by yielding hydroxyl radicals ('OH), we examined whether these oxyradicals are generated in rat striatum during transient focal cerebral ischemia. .OH were detected in dialysate samples by intrastriatal microdialysis coupled with the technique of salicylate hydroxylation. Ischemia was achieved by tandem occlusion of the left middle cerebral artery and common carotid arteries (45 min) followed by reperfusion. An .OH formation occurred both during ischemia and early reperfusion. Additionally, the volume of the striatal infarct induced by ischemia correlated positively with the amount of .OH produced during ischemia and reperfusion. Taken together, these results provide evidence of the formation of cytotoxic .OH in rat striatum which might participate in the ischemic injury of this structure.