| Objective:To investigate the mechanism of hyperglycemia on brainfollowing global ischemia - reperfusion.Methods Cardiac arrest was induced by asphyxiation in rats andresuscitation efforts were begun 7 minutes after arrest. 40 male Wistarrats were randomly divided into 5 groups: sham control group;normglycemic 24h group and hyperglycemic 24h group (the sample weretaken at 24h postresuscitation); normglycemic 72h group andhyperglymic 72h groups (the sample were taken at 72h postresuscitation);each group is equal to 8 (n = 8). Hyperglycemia was induced beforeischemi a by intraperitoneal dextrose administration, Myeloperoxidase(MPO) immunohistochemistry was used to ascertain the neutrophildeposition in brain at 24h and 72h after cardiopulmonary resuscitation.The neurological status was evaluated daily for 3 days after CPR.Result: Brain of sham-operated animals contained almost no MPOactivity. Neutrophils in brain of normoglycemic-ischemia animals weredistributed diffusely. By contrast, striking numbers of MPO-positive cellwere present in brain after hyperglycemia ischemia. The neurologicalscore of hyperglycemia animals was significantly worse than that of shamcontrol and normglycemic-ischemic groups.Conclusion: Hyperglycemia triggers the early, massive deposition ofneutrophils in the postischemic global brain, which is an important eventthat may contribute to exacerbate global ischemia-reperfusion injury. |
PDF Full Text Request