Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats

Myeloperoxidase (MPO) immunohistochemistry was used to ascertain the role of polymorphonuclear leukocytes in hyperglycemia-induced accentuation of brain injury after transient ischemia. Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. Hyperglycemia was induced before ischemia by intraperitoneal dextrose administration. Quantitative MPO immunohistochemistry was performed at 24 h and 3 days postischemia. Brains of normoglycemic-ischemic animals contained almost no MPO activity. By contrast, striking numbers of MPO-positive cells were present in brains studied 24 h after hyperglycemic ischemia, both within pial and parenchymal vessels and within the parenchyma. MPO deposition tended to subside at 3 days. These results indicate that hyperglycemia triggers the early, massive deposition of neutrophils in the postischemic brain--an event that may contribute to exacerbation of injury.