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Normobaric hyperoxia reduces MRI diffusion abnormalities and infarct size in experimental stroke.
Aneesh B Singhal1, Rick M Dijkhuizen, Bruce R Rosen
1Neuroprotection Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA. asinghal@partners.org
Neurology
|March 27, 2002
Summary
Normobaric hyperoxia (100% oxygen) shows neuroprotective effects in stroke models. Early administration, within 30 minutes, significantly reduces brain damage, particularly in the cerebral cortex, highlighting a critical therapeutic time window.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Medical Imaging
Background:
- Hyperbaric oxygen therapy is a recognized stroke treatment.
- Investigating normobaric oxygen's neuroprotective potential and optimal timing is crucial.
Purpose of the Study:
- To evaluate the neuroprotective effects of normobaric hyperoxia in a rat stroke model.
- To determine the therapeutic time window for normobaric oxygen administration.
Main Methods:
- Diffusion- and perfusion-weighted MRI (DWI/PWI) assessed brain injury after middle cerebral artery occlusion (MCAO) in rats.
- Rats received either 30% (normoxia) or 100% (hyperoxia) oxygen.
- Lesion volumes were analyzed after MCAO with hyperoxia initiated at 15, 30, or 45 minutes post-occlusion.
Main Results:
- Hyperoxia improved apparent diffusion coefficient (ADC) values in cortical border zones, indicating tissue recovery.
- While hyperoxia initially reduced ADC lesion volumes, they later increased.
- Administering 100% oxygen within 30 minutes significantly reduced 48-hour total and cortical lesion volumes.
- Striatal lesion volumes were significantly reduced when hyperoxia was initiated 15 minutes after MCAO.
Conclusions:
- Normobaric hyperoxia administered within 30 minutes of transient stroke salvages ischemic brain tissue in rats.
- Neuroprotection is enhanced when treatment is initiated earlier, emphasizing the importance of prompt intervention.