Razi Journal of Medical Sciences

  Background & Aim: Ischemic preconditioning (IPC) is an endogenous phenomenon that can induce ischemic tolerance (IT) in a variety of organs such as brain. In this study, we examined the intermittent and prolonged effects of normobaric hyperoxia (HO) on neurologic deficit scores, infarct volume, and glutathione peroxidase activity.

  Material and Method: This experimental study was done in Shahid Beheshti University. The rats were divided into four main groups. The first two main groups were exposed to HO in prolonged (24hrs PrHO) and intermittent (4hrs×6days InHO) ways and the second two groups acted as controls and were exposed to 21% oxygen in the same chamber (room air, RA) continuously (24hrs PrRA) and discontinuously (4hrs×6days InRA). Each group was divided into three subgroups. After 24 hours,the first subgroup was subjected to a 60-minute MCAO followed by 24hrs of reperfusion. Then,the IT induced by InHO and PrHO was measured through neurologic deficit scores and infarct volume. The second and third subgroups were called sham ^__ operated and intact subgroups ^__ and used for the assessment of the effect of HO on glutathione peroxidase activity. Enzyme activities, arterial blood gases, and infarct volume were compared using one-way ANOVA test. The neurologic deficit scores were analyzed using the Mann-Whitney U test.

  Results: Our findings indicate that InHO and PrHO are involved in the induction of IT. Pretreatment with InHO and PrHO can reduce neurologic deficit scores and infarct volume and increase glutathione peroxidase activity significantly. The catalase activity of prolonged HO groups was significantly more than that of intermittent HO groups.

  Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, InHO and PrHO seem to partly exert their effects via increasing glutathione peroxidase activity.