AI Article Synopsis
- Recent research indicates that normobaric hyperoxia (HO) can help reduce brain injury caused by lack of oxygen in a rat stroke model.
- Rats were divided into two groups: one received 95% oxygen for 4 hours daily, while the control group received normal air (21% oxygen) before undergoing a stroke simulation.
- Results showed that those treated with HO had better neurological outcomes and increased expression of certain sodium-calcium exchangers (NCX), suggesting a potential protective mechanism against ischemic injury.
Article Abstract
Background: Recent studies suggest that normobaric hyperoxia (HO) reduces hypoxia-reoxygenation injury in the rat brain. We have attempted to determine the effect of HO on Na(+)-Ca(2+) exchangers (NCX) in the rat stroke model.
Methods: Rats were divided into two experimental groups. The first group was exposed to 95% inspired HO for 4h/day for 6 consecutive days (HO). The second group acted as the control, and was exposed to 21% oxygen in the same chamber. Each main group was subdivided to middle cerebral artery occlusion (MCAO-operated) and intact (without any surgery) subgroups. After 48 h from pretreatment, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24h reperfusion, neurologic deficit score (NDS) and infarct volume were measured in MCAO-operated subgroups. The NCXs expression levels of the core, penumbra and subcortical regions were assessed in sham-operated and intact subgroups.
Result: Preconditioning with HO decreased NDS and infarct volume, and increased the expression of NCX1, NCX2 and NCX3 in the penumbra, NCX2, NCX3 in the core and NCX1 and NCX3 in the subcortex.
Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, HO partly is associated with the expression of NCX1, 2, 3 consistent with an active role in the genesis of ischemic protection.
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| http://dx.doi.org/10.1016/j.neuroscience.2013.01.064 | DOI Listing |
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