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From the Neuroprotection Research Laboratory (Drs. Singhal, Dijkhuizen, and Lo) and NMR Center (Drs. Dijkhuizen and Rosen), Departments of Neurology and Radiology, Massachusetts General Hospital, and Program in Neuroscience, Harvard Medical School, Charlestown, MA.
Address correspondence and reprint requests to Dr. Aneesh B. Singhal, MGH East 149-2322, Charlestown, MA 02129; e-mail: asinghal{at}partners.org
Background: Hyperbaric oxygen therapy is considered an important stroke treatment strategy.
Background: To determine whether normobaric oxygen is neuroprotective, and, if so, what the therapeutic time window is.
Methods: Experiment 1—Serial diffusion- and perfusion-weighted MRI (DWI and PWI) was performed after middle cerebral artery filament occlusion (MCAO) in rats randomized to FiO2 30% (normoxia) or FiO2 100% (hyperoxia). Experiment 2—48-hour lesion volumes were analyzed in rats subjected to 2-hour MCAO and randomized to normoxia or hyperoxia starting 15, 30, or 45 minutes after MCAO and ending 15 minutes after reperfusion.
Results: Experiment 1—Lesion apparent diffusion coefficient (ADC) values were persistently low in normoxic animals. In hyperoxia-treated rats, ADC values in cortical border zones showed progressive recovery from 66 ± 3% of contralateral before hyperoxia, to 104 ± 20% at 
2 hours. Striatal ADC values showed early but ill-sustained improvement. ADC lesion volumes increased progressively in the normoxia group. In the hyperoxia group, ADC lesion volumes tended to decrease after starting hyperoxia; however, lesions later increased in size, and 2-hour lesion volumes were not significantly different from baseline. PWI showed stable right MCA hypoperfusion in all animals. Experiment 2—Hyperoxia within 30 minutes significantly reduced total and cortical lesion volumes at 48 hours after stroke. Striatal lesion volumes were significantly reduced in the hyperoxia-15 group.
Conclusion: In rats subjected to transient stroke, 100% oxygen administered within 30 minutes salvages ischemic brain tissue, especially in the cerebral cortex. Reducing the time to treatment enhances the degree of neuroprotection.
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