Journal
CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES
Volume 34, Issue 3, Pages 356-361Publisher
CANADIAN JOURNAL NEUROLOGICAL SCIENCES INC
DOI: 10.1017/S031716710000682X
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Funding
- NICHD NIH HHS [HD43120, R01 HD043120] Funding Source: Medline
- NIGMS NIH HHS [R25 GM060507-02, R25 GM060507, R25 GM060507-01A1] Funding Source: Medline
- NIMHD NIH HHS [P20 MD001632-02, P20 MD006988, P20 MD001632, 5P20MD001632] Funding Source: Medline
- NINDS NIH HHS [R01 NS043338, R21 NS052492, R01 NS045694, NS52492, NS45694, NS53407, NS43338, R01 NS053407] Funding Source: Medline
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Background: Oxidative stress largely contributes to early brain injury after subarachnoid hemorrhage (SAH). One of the major sources of reactive oxygen species is NADPH oxidase, upregulated after SAH. We hypothesized that NADPH oxidase-induced oxidative stress plays a major causative role in early brain injury after SAH. Methods: Using gp91(phox) knockout (ko) and wild-type (wt) mice, we studied early brain injury in the endovascular perforation model of SAH. Mortality rate, cerebral edema, oxidative stress, and superoxide production were measured at 24 h after SAH. Neurological evaluation was done at 23 h after SAH surgery. Results: Genotyping confirmed the existence of a nonfunctional gp91(phox) gene in the ko mice. CBF measurements did not show differences in SAH-induced acute ischemia between ko and wt mice. SAH caused a significant increase of water content in the ipsilateral hemisphere as well as an increase of Malondialdehyde (MDA) levels and superoxide production. There were no significant differences in post-SAH mortality rate, brain water content and the intensity of the oxidative stress between knockout and wild type groups of mice. Conclusions: Our results suggest that gp91(phox) is not critically important to the early brain injury after SAH. An adaptive compensatory mechanism for free radical production in knockout mice is discussed.
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