Reduction of the neurological deficit in mice with traumatic brain injury by nitric oxide synthase inhibitors
Autor: | Christian Mésenge, Michel Plotkine, Catherine Verrecchia, Roger R. Boulu, Monique Allix |
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Rok vydání: | 1996 |
Předmět: |
Male
Indazoles Time Factors Traumatic brain injury Neurological disorder Pharmacology Motor Activity Arginine Neuroprotection Drug Administration Schedule Nitric oxide Central nervous system disease chemistry.chemical_compound Mice medicine Animals Enzyme Inhibitors Neurologic Examination Analysis of Variance biology Dose-Response Relationship Drug business.industry medicine.disease Nitric oxide synthase NG-Nitroarginine Methyl Ester Neuroprotective Agents chemistry Enzyme inhibitor Brain Injuries Closed head injury biology.protein Neurology (clinical) Nitric Oxide Synthase business Neuroscience |
Zdroj: | Europe PubMed Central |
ISSN: | 0897-7151 |
Popis: | This study investigates the effect of the NO synthase inhibitors, NG-nitro L-arginine methyl ester (L-NAME) and 7-nitro indazole (7-NI), on the neurological deficit 24 h after a moderate closed head injury in mice. Low doses of L-NAME or 7-NI given soon after the injury significantly reduced the neurological deficit compared to the vehicle-treated group. L-Arginine (300 mg/kg) did not alter the neurological deficit, but reversed the protective effects of both L-NAME and 7-NI when given at the same time. Both L-NAME and 7-NI had dose-related effects. The neuroprotective effects of L-NAME and 7-NI occurred when the drugs were given 5, 30, or 60 min after brain injury, but not when treatment was begun 2 h after brain injury, suggesting a short therapeutic window for both drugs. These results suggest that NO synthesis by neuronal NO synthase plays an important role in the early neurotoxic cascade leading to neurological deficit following traumatic brain injury. |
Databáze: | OpenAIRE |
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