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Pathogenesis of hypoxic-ischemic brain injury in a perinatal rodent model

dc.contributor.authorSilverstein, Faye Sarahen_US
dc.contributor.authorBuchanan, Karenen_US
dc.contributor.authorJohnston, Michael V.en_US
dc.date.accessioned2006-04-07T18:24:30Z
dc.date.available2006-04-07T18:24:30Z
dc.date.issued1984-08-31en_US
dc.identifier.citationSilVerstein, Faye, Buchanan, Karen, Johnston, Michael V. (1984/08/31)."Pathogenesis of hypoxic-ischemic brain injury in a perinatal rodent model." Neuroscience Letters 49(3): 271-277. <http://hdl.handle.net/2027.42/24718>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6T0G-485YHN1-1H5/2/33213478bb58e67825b2ac2bff459a07en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/24718
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6493609&dopt=citationen_US
dc.description.abstractExposure of immature rats to 8% oxygen after unilateral carotid artery ligation (UCL) causes metabolic, neurochemical and histopathological changes in the ipsilateral forebrain that resemble those in human perinatal hypoxic-ischemic encephalopathy. Regional cerebral perfusion in this model was examined by visual analysis of India ink trapped in cerebral vessels and measurement of [14C]iodoantipyrine ([14C]IAP) and [3H]flunitrazepam extraction into the brain. UCL alone reduced [14C]IAP accumulation in the ipsilateral hemisphere by 20% and hypoxia superimposed on UCL progressively reduced ipsilateral hemisphere perfusion by 71% at 2 h. Hypoxia probably injures neurons in this model by causing a critical reduction in cerebral perfusion, an effect which also appears to be important in the human disorder.en_US
dc.format.extent352366 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titlePathogenesis of hypoxic-ischemic brain injury in a perinatal rodent modelen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbsecondlevelPsychologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbtoplevelSocial Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumCenter for Human Growth and Development, Ann Arbor, MI 48109, U.S.A.; Department of Pediatrics and Neurology, University of Michigan Medical School, Ann Arbor, MI 48109, U.S.A.en_US
dc.contributor.affiliationumCenter for Human Growth and Development, Ann Arbor, MI 48109, U.S.A.; Department of Pediatrics and Neurology, University of Michigan Medical School, Ann Arbor, MI 48109, U.S.A.en_US
dc.contributor.affiliationumDepartment of Pediatrics and Neurology, University of Michigan Medical School, Ann Arbor, MI 48109, U.S.A.; Center for Human Growth and Development, Ann Arbor, MI 48109, U.S.A.en_US
dc.identifier.pmid6493609en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/24718/1/0000140.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0304-3940(84)90301-Xen_US
dc.identifier.sourceNeuroscience Lettersen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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