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dc.contributor.author James, Michael Lucas
dc.contributor.author Wang, Haichen
dc.contributor.author Venkatraman, Dr Talaignair
dc.contributor.author Song, Pingping
dc.contributor.author Lascola, Christopher David
dc.contributor.author Laskowitz, Daniel Todd
dc.date.accessioned 2012-11-01T19:38:29Z
dc.date.available 2012-11-01T19:38:29Z
dc.date.issued 2010-01
dc.identifier.citation Michael L. James, Haichen Wang, Talaignair Venkatraman, Pingping Song, Christopher D. Lascola, and Daniel T. Laskowitz. Journal of Neurotrauma. January 2010, 27(1): 217-228 en_US
dc.identifier.uri http://hdl.handle.net/10161/5971
dc.description.abstract There is emerging evidence to suggest that brain natriuretic peptide (BNP) is elevated after acute brain injury, and that it may play an adaptive role in recovery through augmentation of cerebral blood flow (CBF). Through a series of experiments, we tested the hypothesis that the administration of BNP after different acute mechanisms of central nervous system (CNS) injury could improve functional recovery by improving CBF. C57 wild-type mice were exposed to either pneumatic-induced closed traumatic brain injury (TBI) or collagenase-induced intracerebral hemorrhage (ICH). After injury, either nesiritide (hBNP) (8 μg/kg) or normal saline were administered via tail vein injection at 30 min and 4 h. The mice then underwent functional neurological testing via rotorod latency over the following 5 days and neurocognitive testing via Morris water maze testing on days 24–28. Cerebral blood flow (CBF) was assessed by laser Doppler from 25 to 90 min after injury. After ICH, mRNA polymerase chain reaction (PCR) and histochemical staining were performed during the acute injury phase (<24 h) to determine the effects on inflammation. Following TBI and ICH, administration of hBNP was associated with improved functional performance as assessed by rotorod and Morris water maze latencies (p < 0.01). CBF was increased (p < 0.05), and inflammatory markers (TNF-α and IL-6; p < 0.05), activated microglial (F4/80; p < 0.05), and neuronal degeneration (Fluoro-Jade B; p < 0.05) were reduced in mice receiving hBNP. hBNP improves neurological function in murine models of TBI and ICH, and was associated with enhanced CBF and downregulation of neuroinflammatory responses. hBNP may represent a novel therapeutic strategy after acute CNS injury. en_US
dc.publisher Mary Ann Liebert en_US
dc.relation.isversionof doi:10.1089/neu.2009.1022 en_US
dc.title Brain Natriuretic Peptide Improves Long-Term Functional Recovery after Acute CNS Injury in Mice en_US
dc.type Article en_US
duke.description.endpage 228 en_US
duke.description.issue 1 en_US
duke.description.startpage 217 en_US
duke.description.volume 27 en_US
dc.relation.journal Journal of Neurotrauma en_US

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