The effect of prolonged and intermittent normobaric hyperoxia preconditioning on glutathione reductase activity in the rat stroke model

Background: Ischemic preconditioning (IPC) is an endogenous phenomenon that can induce ischemic tolerance (IT) in a variety of organs such as brain. Objective: To investigate the intermittent and prolonged dose of normobaric hyperoxia (HO) on neurologic deficit scores, infarct volume, and glutathione reductase activity. Methods: this was an experimental study carried out in Shahid Beheshti University of Medical Sciences in Tehran, Iran. A total of 80 rats were initially divided into four main groups. The first two groups were exposed to HO in prolonged (24h PrHO 95% O2) and intermittent (4h×6days InHO 95% O2) groups and the second two groups served as controls and exposed to 21% oxygen in the same chamber (room air, RA) continuously (24h PrRA) and discontinuously (4h×6days InRA). Each group was further subdivided into three subgroups. After 24 h, the first subgroup was subjected to 60 minutes middle cerebral artery occlusion (MCAO) followed by 24h of reperfusion. Later, the IT induced by InHO and PrHO, were measured by neurologic deficit scores and infarct volume. The second and third subgroups were marked as sham-operated and intact subgroups for assessing the effect of HO on glutathione reductase activity. Findings: Our findings indicated that the InHO and PrHO are involved in induction of IT. Pre-treatment with InHO and PrHO reduced the neurologic deficit scores and infarct volume, significantly. The InHO and PrHO caused a significant increase in glutathione reductase activity. The catalase activity of prolonged HO groups was significantly higher than that of intermittent HO groups. Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, the InHO and PrHO seem to partly exert their effects via increased glutathione reductase activity.