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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
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. (Anaesthesiology and Intensive Care)
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. (Anaesthesiology and Intensive Care)
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2006 (Engelska)Ingår i: Acta neurochirurgica. Supplement, ISSN 0065-1419, Vol. 96, s. 288-294Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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

Ort, förlag, år, upplaga, sidor
2006. Vol. 96, s. 288-294
Nyckelord [en]
Animals, Antibodies/*administration & dosage, Blood-Brain Barrier/*drug effects/physiopathology, Brain Edema/physiopathology/*prevention & control, Brain Injuries/complications/diagnosis/*drug therapy/physiopathology, Gait Disorders; Neurologic/diagnosis/etiology/physiopathology/*prevention & control, Injections; Intraventricular, Male, Nitric Oxide Synthase Type I/*antagonists & inhibitors/*immunology, Rats, Rats; Sprague-Dawley, Research Support; Non-U.S. Gov't, Treatment Outcome
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Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:uu:diva-20199PubMedID: 16671473OAI: oai:DiVA.org:uu-20199DiVA, id: diva2:47972
Tillgänglig från: 2006-12-06 Skapad: 2006-12-06 Senast uppdaterad: 2010-10-21Bibliografiskt granskad

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