Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/66881
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dc.contributor.authorBarry, C.en
dc.contributor.authorHelps, S.en
dc.contributor.authorVan Den Heuvel, C.en
dc.contributor.authorVink, R.en
dc.date.issued2011en
dc.identifier.citationBrain Research, 2011; 1389:143-151en
dc.identifier.issn0006-8993en
dc.identifier.issn1872-6240en
dc.identifier.urihttp://hdl.handle.net/2440/66881-
dc.description.abstractBACKGROUND: Raised intracranial pressure (ICP) following SAH predicts poor outcome and is due to hemorrhage volume and possibly, brain edema, hydrocephalus and increased volume of circulating intracranial blood. Interventions that reduce edema may therefore reduce ICP and improve outcome. The neuropeptide substance P (SP) mediates vasogenic edema formation in animal models of ischemic stroke, intracerebral hemorrhage and brain trauma, and may contribute to development of increased ICP. SP (NK1 tachykinin receptor) blockade using n-acetyl-l-tryptophan (NAT) reduces edema and improves outcome in these models. This study therefore assessed whether SP mediates edema formation in experimental SAH. METHODS: SAH was induced in rats by either injection of autologous blood into the prechiasmatic cistern (injection SAH) or by arterial puncture of the Circle of Willis (filament SAH). NAT was injected (i.v.) 30min after SAH induction. Subgroups were assessed for brain water content, SP and albumin immunoreactivity, and functional outcome at 5, 24 and 48h or ICP over 5h. RESULTS: A secondary ICP increase occurred within 2h of SAH. Brain edema followed filament SAH (p<0.001) and correlated with functional deficits (r=0.8, p<0.01). Increased albumin immunoreactivity (p<0.001) indicated vasogenic edema. However, NAT treatment did not improve ICP, edema or outcome. CONCLUSIONS: Experimental SAH produced secondary ICP elevation, vasogenic brain edema and functional deficits, although it is unclear if edema contributed to ICP. Blockade of SP did not improve any outcome parameters, suggesting that neurogenic inflammation may be less critical than other factors in these models.en
dc.description.statementofresponsibilityChristine M. Barry, Stephen C. Helps, Corinna van den Heuvel, Robert Vinken
dc.language.isoenen
dc.publisherElsevier Science Bven
dc.rightsCopyright © 2011 Elsevier B.V. All rights reserved.en
dc.subjectSubarachnoid hemorrhage; Brain edema; Substance P; Neurological outcome; Intracranial pressureen
dc.titleCharacterizing the role of the neuropeptide substance P in experimental subarachnoid hemorrhageen
dc.typeJournal articleen
dc.identifier.rmid0020110807en
dc.identifier.doi10.1016/j.brainres.2011.02.082en
dc.identifier.pubid28681-
pubs.library.collectionPathology publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidVan Den Heuvel, C. [0000-0001-7264-4655]en
dc.identifier.orcidVink, R. [0000-0002-4885-0667]en
Appears in Collections:Pathology publications

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