Abstract
Background. Hyperglycemia exacerbates focal ischemic brain damage supposedly through various mechanisms. One such mechanism is oxidative stress involving reactive oxygen and nitrogen species (RONS) production. Nitrones attenuate oxidative stress in various models of brain injury. Sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) can be administered experimentally and has been shown to be neuroprotective in experimental brain trauma.Aims of the study. We hypothesized that S-PBN might be neuroprotective in hyperglycemic focal cerebral ischemia.Material and methods. Rats were made hyperglycemic by an intraperitoneal bolus injection of glucose (2 g/kg) and then subjected to 90 min transient middle cerebral artery occlusion (MCAO). They were randomized to a therapeutic regime of S-PBN (156 mg/kg) or saline given intravenously. Neurological testing according to Bederson and tetrazolium red staining were performed after 1 day.Results. S-PBN improved the neurological performance at day 1 both in Bederson score (1.3 ± 0.8 versus 2.7 ± 0.48) and on the inclined plane (74.5% ± 4.6 (S-PBN) versus 66% ± 8.3 (control), P < 0.05) but did not reduce the infarct size. Physiological data did not differ between groups.Conclusion. S-PBN may improve neurological performance at short-term survival (1 day) in the present model of hyperglycemic-ischemic brain injury in rats. This effect appeared not to be primarily related to reduced infarct size.
Highlights
Ischemic stroke is a common and life-threatening neurological disease with substantial morbidity and mortality
A total of 42 rats were successfully subjected to middle cerebral artery occlusion (MCAO); 23 rats were excluded due to either subarachnoid hemorrhage (SAH) on post-mortem examination or postoperative mortality not attributed to SAH
The present results indicate that sulfophenyl-N-tert-butyl nitrone (S-phenyl-N-tert-butyl nitrone (PBN)) may ameliorate hyperglycemic-ischemic brain damage by other mechanisms than reducing the infarct size, since only neurological performance was improved after 1 day of survival
Summary
Ischemic stroke is a common and life-threatening neurological disease with substantial morbidity and mortality. Hyperglycemia exacerbates focal ischemic brain damage supposedly through various mechanisms One such mechanism is oxidative stress involving reactive oxygen and nitrogen species (RONS) production. Rats were made hyperglycemic by an intraperitoneal bolus injection of glucose (2 g/kg) and subjected to 90 min transient middle cerebral artery occlusion (MCAO) They were randomized to a therapeutic regime of S-PBN (156 mg/kg) or saline given intravenously. S-PBN may improve neurological performance at short-term survival (1 day) in the present model of hyperglycemic-ischemic brain injury in rats. This effect appeared not to be primarily related to reduced infarct size
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