Time course of neuroprotection induced by normobaric hyperoxia in focal cerebral ischemia.

Background: The purpose of this study was to determine if normobaric hyperoxia (HO) preconditioning offers durable neuroprotection against cerebral ischemia and the role of reactive oxygen species in the ischemic tolerance mechanism.

Materials And Methods: Rats were divided into four experimental main groups. First main group which was comprised four subgroups, were exposed to 90% HO for 6 days, 4 hours per day and subjected to 60 minutes of right middle cerebral artery occlusion (MCAO) after 2, 5, 10, and 15 days. Second group acted as control, was exposed to 21% oxygen (RA; room air) in the same chamber, and subjected to 60 minutes of right MCAO. Third main group comprised two subgroups, were exposed to 90% HO for 6 days, 4 hours per day, received normal saline (NS; 2HO+NS) and dimethylthiourea (DT) just before inhaling 90% HO (2HO+DT). Forth main group was exposed to 21% oxygen (2RA) in the same chamber and received normal saline (2RA+NS) and DT just before inhaling 21% oxygen (2RA+DT). Last two main groups were subjected to 60 minutes of right MCAO after 2 days. After 24-hour reperfusion, neurological deficit score (NDS), infarct volume, brain water content, and Evans blue extravasations were assessed in all animals.

Results: First main group compared with the RA group, NDS, infarct volume, Brain water content, and Evans blue extravasations were reduced in 2, 5, and 10 days significantly, whereas there was no difference among groups 2HO+DT, 2RA+DT, and 2RA+NS.

Conclusions: In the model of transient focal cerebral ischemia, hyperoxia preconditioning induced effective but transient neuroprotective effects.