Intracerebral administration of neuronal nitric oxide synthase antiserum attenuates traumatic brain injury-induced blood-brain barrier permeability, brain edema formation, and sensory motor disturbances in the rat
作者： Hari S. Sharma , L. Wiklund , R. D. Badgaiyan , S. Mohanty , P. Alm
关键词:
摘要: The role of nitric oxide (NO) in traumatic brain injury (TBI)-induced sensory motor function and pathology was examined using intracerebral administration neuronal synthase (nNOS) antiserum a rat model. TBI produced by making longitudinal incision into the right parietal cerebral cortex limited to dorsal surface hippocampus. Focal induces profound edematous swelling, extravasation Evans blue dye, up-regulation nNOS injured underlying subcortical areas at 5 hours. traumatized animals exhibited pronounced deficit, as seen Rota-Rod grid-walking tests. Intracerebral (1 : 20) minutes 1 hour after significantly attenuated edema formation, leakage, expression regions. antiserum-treated rats showed improved functions. However, 2 hours did not influence these parameters significantly. These novel observations suggest that NO participates blood-brain barrier disruption, disturbances early phase TBI, has some potential therapeutic value requiring additional investigation.
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