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Updated: Apr 20, 2026

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
Delayed reperfusion deficits after experimental stroke account for increased pathophysiology
Fiona E Burrows1, Natasha Bray1, Adam Denes2
1The University of Manchester, Faculty of Life Sciences, Manchester, UK.
Cerebral blood flow, specifically oxyhemoglobin (HbO2), drops during ischemic stroke and initially recovers post-reperfusion. However, delayed inflammation causes a secondary decline, indicating a potential therapeutic target for stroke recovery.
Area of Science:
- Neuroscience
- Biomedical Engineering
- Cerebrovascular Research
Background:
- Cerebral blood flow and oxygenation post-ischemic stroke are critical but poorly understood.
- Therapeutic interventions require precise knowledge of oxygenation dynamics after reperfusion.
Purpose of the Study:
- To investigate changes in cortical oxyhemoglobin (HbO2) concentration during and after ischemic stroke.
- To correlate cortical injury and inflammation with delayed oxygen perfusion deficits.
Main Methods:
- Multispectral optical imaging in anesthetized mice subjected to middle cerebral artery occlusion (MCAo).
- Immunohistochemistry to assess cortical injury and markers of inflammation.
- Pathlength scaling algorithm to calculate oxygenation maps.
Main Results:
- MCAo group showed a significant HbO2 drop during occlusion, followed by an initial increase post-reperfusion.
- Over 6 hours, HbO2 levels declined below pre-stroke levels, indicating a delayed deficit.
- Inflammation markers correlated with delayed reperfusion deficits, not the initial HbO2 drop.
Conclusions:
- Despite initial reperfusion, a delayed compromise in cerebral oxygenation occurs after ischemic stroke.
- This delayed deficit coincides with neuroinflammation and presents a potential therapeutic target.
- Targeting inflammation may improve stroke outcomes after thrombolysis.
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