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Acta Neurochir Suppl. 2013;118:83-7. doi: 10.1007/978-3-7091-1434-6_14.

Cerebral hemorrhage, brain edema, and heme oxygenase-1 expression after experimental traumatic brain injury.

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  • 1Department of Neurosurgery, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.


Intracranial bleeding is a common and serious consequence of traumatic brain injury (TBI). In the present study, we investigated cerebral hematoma occurrence, brain edema formation, blood-brain barrier (BBB) disruption, and heme oxygenase-1 (HO-1) expression after TBI. Moderate severity (1.8-2.2 atmospheres [ATM]) TBI was induced by lateral fluid percussion in male adult Sprague-Dawley rats. Sham rats underwent only a craniotomy. Rats were euthanized 24 h later for brain histology and immunoblotting analysis. We found TBI-induced cerebral hematomas and iron deposition in the ipsilateral hemisphere in all rats. TBI also caused marked BBB disruption (p < 0.05) and brain swelling (p < 0.05). HO-1, a key enzyme for heme degradation, was upregulated significantly after TBI (419 ± 89 vs 194 ± 59 pixels in the sham, p < 0.05). These results suggest that cerebral hematomas might play a role in brain injury after TBI. Future studies should determine the role of iron released from the cerebral hematoma in TBI.

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