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Objective: Ischemic preconditioning (IPC) is an endogenous phenomenon that can induce ischemic tolerance (IT) in variety of organs such as brain. In this study, we examined the intermittent and prolonged normobaric hyperoxia (HO) on neurologic deficit scores, infarct volume, and superoxide dismutase activity. Materials and Methods: The rats were divided to four main groups. First two main groups were exposed with HO in prolonged (24 h; PrHO) and intermittent (4 h×6 days; InHO) groups and second two main group acted as controls, and were exposed to 21% oxygen in the same chamber (room air, RA) continuously (24 h; PrRA) and discontinuously (4 h×6 days; InRA). Each group subdivided to three subgroups. After 24 h, first subgroup were subjected to 60 minutes MCAO followed by 24 h of reperfusion. Then, IT induced by InHO and PrHO were measured by neurologic deficit scores and infarct volume. Second and third subgroups were called sham-operated and intact subgroups for assessment of the effect of HO on superoxide dismutase activity. Results: Our findings indicate that InHO and PrHO are involved in the induction of IT. Pretreatment with InHO and PrHO reduced neurologic deficit scores and infarct volume significantly. InHO and PrHO increase superoxide dismutase activity significantly. Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, InHO and PrHO seem to partly exert their effects via increase superoxide dismutase activity.

Keywords: Ischemic preconditioning, Normobaric Hyperoxia, Superoxide dismutase enzyme activity, stroke

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