Reduction of Superoxide Dismutase Activity Correlates with Visualization of Edema by T2-weighted MR Imaging in Focal Ischemic Rat Brain
Autor: | Philip Weinstein, Yoram Cohen, Pak H. Chan, Lee Hong Chang, Takashi Yoshimoto, Thomas L. James, Shigeki Imaizumi |
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Rok vydání: | 1994 |
Předmět: |
chemistry.chemical_classification
Pathology medicine.medical_specialty biology business.industry Cerebral infarction Cerebrum Glutathione peroxidase Ischemia medicine.disease Superoxide dismutase medicine.anatomical_structure chemistry Edema medicine.artery Cortex (anatomy) biology.protein Medicine Surgery Neurology (clinical) Common carotid artery medicine.symptom business |
Zdroj: | Neurologia medico-chirurgica. 34:1-9 |
ISSN: | 1349-8029 0470-8105 |
DOI: | 10.2176/nmc.34.1 |
Popis: | This study investigated the correlation between in vivo serial T2-weighted magnetic resonance (MR) imaging and changes in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and water, sodium ion (Na+), and potassium ion (K+) contents measured in vitro using rat brain following right middle cerebral artery occlusion in conjunction with bilateral common carotid artery (CCA) occlusion. One hour later the left CCA was released. Serial MR images showed edema developed from the outer cortex towards the center. The T2 signal intensity of the injured right cortex increased with time compared to that of the contralateral cortex. Increased Na+ and water and decreased K+ contents occurred in the injured cortex, indicating that serial T2-weighted MR imaging reflects the changes in water content and Na+ and K+ concentrations determined by biochemical techniques. GSH-Px activity was little changed. Total SOD in the injured cortex decreased 1 hour after ischemia and remained low throughout the experiment. In contrast, SOD activity in the noninfarcted left cortex also decreased after 1 hour but returned to normal after 2 hours of ischemia. Our results suggest that oxygen free radicals are important in developing ischemic brain edema and cerebral infarction. |
Databáze: | OpenAIRE |
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