Effects of hyperglycemia on cerebral blood flow and edema formation after carotid artery occlusion in Fischer 344 rats.

This study examines whether during bilateral carotid artery occlusion in Fischer 344 rats, hyperglycemia induces cerebrovascular changes that enhance brain edema formation. Preischemic hyperglycemia was induced by intraperitoneal administration of D-glucose solution. Laser-Doppler flowmetry, indicated that after the initial decline in blood flow with carotid occlusion (36 +/- 4% of preischemic), hyperglycemic but not control rats showed a further progressive decrease to 19 +/- 2% of preischemic at 120 minutes (p < 0.001). Brain water content was significantly higher in hypercompared to normoglycemic rats after both 2 hours of permanent occlusion (3.86 +/- 0.05 vs. 3.73 +/- 0.03 g/g dry wt.; p < 0.05) and 2 hours of temporary occlusion followed by 1 hour of reperfusion (4.01 +/- 0.08 vs. 3.71 +/- 0.03 g/g dry wt.; p < 0.05). The difference in brain edema formation between normo- and hyperglycemic rats appears to primarily reflect the effects of hyperglycemia on CBF. Cerebral plasma volume (CPV) 2 hours after occlusion was also reduced in hyper-compared to normoglycemic rats (3.9 +/- 0.9 and 7.2 +/- 0.1 microliters/g; p < 0.01). Thus, hyperglycemia in a model of global ischemia induces a reduction in CPV and progressive decline in CBF. In this model, the decline in CBF is of sufficient magnitude to enhance brain injury as evidenced by edema formation.