Focal Cerebral Ischemia / Reperfusion Injury In Experimental Pathology,

We investigated how ischemic tissue can be salvaged by reperfusion and how the temeral profile of ischemic tissue damage and neutropil response are after transient middle cerebral artery occlusion in the rat. The lesion size increased progressively with increasing occlusion time, up to 4h, when the lesions were as extensive as those observed following 24h of permanent occlusion. Neutrophil infiltration into tissue and the time of peak neutrophil infiltration were 12h and 24h. IgG and C3c immunoactivities in the ischemic lesion area were detected using immunchis-tochemistry. Both the administration of ibuprofen and complement depletion with cobra venom factor reduced neutrophil infiltration and decreased brain ischemic lesion- Normal serum deteriorated the damage of ischemia — like condition to cultured neurons while depleted serum had no such effect.The results above indicated that reperfusion beyond the time window can not salvage ischemic brain tissue. Neutrophil infiltration increases sharply between 12h and 24h after transient middle cerebral artery occlusion and early adminstration of ibuprofen can decrease ischemic brain damage by reducing neutrophil infiltration. It is suggested that complement system is activated during cerebral ischemia/reperfusion and contributes to ischemic brain damage by either nectrophil mediated effects or cytolytic effect of membrane attack complex.