OBJECTIVES: Recent studies have revealed that nitric oxide (NO) in concert with lipid peroxidation (LP) may play an important role in pathophysiological mechanism(s) of cerebral ischemia. In addition, hyperglycemia exaggerates the pathological changes during cerebral ischemia. The purpose of this study was to investigate the effects of vitamin E (VE) on LP, NO production, and superoxide dismutase (SOD) expression in hyperglycemic rats after cerebral ischemiareperfusion injury. MATERIALS AND METHODS: Malondialdehyde (MA) (indicator of LP) in plasma and brain tissue, total nitrite/nitrate (metabolites of nitric oxide) in plasma, nitrite in brain tissue, and SOD in red blood cells were detected and the results were compared before and after VE administration in hyperglycemic rats with cerebral ischemia-reperfusion injury induced by two common carotid artery occlusions. RESULTS: Ischemia-reperfusion injury together with hyperglycemia caused elevation in NO metabolites and MA levels and this elevation was more p rominent in hyperglycemic rats. SOD was also increased in ischemiareperfusion, and VE administration had positive effects on the SOD level. In addition, VE administration caused a significant decrease in NO metabolite levels after ischemia-reperfusion injury. CONCLUSIONS: These results suggest that prophylaxis with VE may have positive effects on reducing cerebral damage after stroke in patients with diabetes mellitus.
OBJECTIVES: Recent studies have revealed that nitric oxide (NO) in concert with lipid peroxidation (LP) may play an important role in pathophysiological mechanism(s) of cerebral ischemia. In addition, hyperglycemia exaggerates the pathological changes during cerebral ischemia. The purpose of this study was to investigate the effects of vitamin E (VE) on LP, NO production, and superoxide dismutase (SOD) expression in hyperglycemic rats after cerebral ischemiareperfusion injury. MATERIALS AND METHODS:Malondialdehyde (MA) (indicator of LP) in plasma and brain tissue, total nitrite/nitrate (metabolites of nitric oxide) in plasma, nitrite in brain tissue, and SOD in red blood cells were detected and the results were compared before and after VE administration in hyperglycemic rats with cerebral ischemia-reperfusion injury induced by two common carotid artery occlusions. RESULTS:Ischemia-reperfusion injury together with hyperglycemia caused elevation in NO metabolites and MA levels and this elevation was more p rominent in hyperglycemic rats. SOD was also increased in ischemiareperfusion, and VE administration had positive effects on the SOD level. In addition, VE administration caused a significant decrease in NO metabolite levels after ischemia-reperfusion injury. CONCLUSIONS: These results suggest that prophylaxis with VE may have positive effects on reducing cerebral damage after stroke in patients with diabetes mellitus.