The Role of Oxygen Radicals in Reducing Cerebral Edema Caused by Normobaric Hyperoxia Pretreatment in Rat Model of Stroke
Zahedan Journal of Research in Medical Sciences: May 31, 2013, 15 (5); e92967
November 18, 2012
Article Type: Research Article
April 26, 2011
February 23, 2011
M R . The Role of Oxygen Radicals in Reducing Cerebral Edema Caused by Normobaric Hyperoxia Pretreatment in Rat Model of Stroke,
Zahedan J Res Med Sci.
Recent studies have shown that normobaric hyperoxia compared with normobaric normoxia can reduce the damages resulting from the stroke. The purpose of this study is to investigate the effects of oxygen radicals in reduction of cerebral edema caused by normobaric hyperoxia in rat stroke models. Background : Wistar rats were divided into two main experimental groups and were exposed to 90% oxygen (HO) for 4 hours/day during 6 days the main control group was placed inside a special chamber and exposed to room 21% oxygen at 1 atmosphere pressure (RA). Then, each group was divided into three subgroups half an hour before placing and treatment in the oxygen chamber, the first, second and third subgroups of both groups were received no substance (RA and HO), saline (RA-S and HO-S), and dimethylthiourea (RA-MT and HO-MT), respectively in order to evaluate the role of oxygen radicals. Then after 24 hours, they were exposed to ischemia through surgically occlusion of middle cerebral artery in order to create brain edema After 60 minutes of ischemia, the perfusion was reestablished for 24 hours. Then the neurological deficit scores and cerebral edema were analyzed. Materials and Methods : Based on Mann–Whitney U test, the median of recovery effect of neurological deficit was significant ( Results : p<0.05). The extent of cerebral edema, based on one-way ANOVA test, was also significant ( p<0.05). This effect disappeared largely by consumption of dimethylthiourea. The reduction of cerebral edema resulting from normobaric hyperoxia treatment is largely mediated through oxygen radicals.
Cerebral edema; Normobaric hyperoxia; Dimethylthiourea; Neurological deficits; Stroke; Neuroprotection
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