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Oxygen-free radicals in traumatic brain oedema
Y Ikeda1, K L Brelsford, K Ikeda
1Department of Neurological Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Neurological Research
|December 1, 1989
Summary
Oxygen-free radicals contribute to brain edema following injury. While superoxide dismutase did not prevent edema, dimethylthiourea showed a temporary protective effect, suggesting radicals play a role in traumatic brain edema.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Oxygen-free radicals are implicated in ischemic and traumatic conditions.
- Oxygen-free radical scavengers are potential treatments for brain edema.
Purpose of the Study:
- To investigate the effects of superoxide dismutase and dimethylthiourea on cold-induced brain edema in cats.
- To determine if oxygen-free radicals are generated in the brain following cold injury.
Main Methods:
- Vasogenic brain edema was induced via cortical freezing lesions in 44 cats.
- Animals were treated with polyethylene glycol-superoxide dismutase, free superoxide dismutase, or dimethylthiourea.
- Brain water content was measured, and superoxide radicals were detected using nitroblue tetrazolium.
Main Results:
- Neither free nor PEG-superoxide dismutase prevented brain edema development.
- Superoxide radicals were detected in the cold lesion.
- Dimethylthiourea prevented white matter edema at 6 hours but not at 24 hours post-injury.
Conclusions:
- Oxygen-free radicals are generated in the brain after cold injury.
- These radicals are a significant factor in the development of traumatic brain edema.
- Dimethylthiourea offers a transient protective effect against edema formation.