pubmed-article:12621122 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0270611 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0014264 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0332282 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C0185125 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C1512924 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:12621122 | lifeskim:mentions | umls-concept:C1633983 | lld:lifeskim |
pubmed-article:12621122 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:12621122 | pubmed:dateCreated | 2003-4-18 | lld:pubmed |
pubmed-article:12621122 | pubmed:abstractText | Perinatal brain damage is associated not only with hypoxic-ischemic insults but also with intrauterine inflammation. A combination of antenatal inflammation and asphyxia increases the risk of cerebral palsy >70 times. The aim of the present study was to determine the effect of intracisternal (i.c.) administration of endotoxin [lipopolysaccharides (LPS)] on subsequent hypoxic-ischemic brain damage in neonatal rats. Seven-day-old Wistar rats were subjected to i.c. application of NaCl or LPS (5 microg/pup). One hour later, the left common carotid artery was exposed through a midline neck incision and ligated with 6-0 surgical silk. After another hour of recovery, the pups were subjected to a hypoxic gas mixture (8% oxygen/92% nitrogen) for 60 min. The animals were randomized to four experimental groups: 1) sham control group, left common carotid artery exposed but not ligated (n = 5); 2) LPS group, subjected to i.c. application of LPS (n = 7); 3) hypoxic-ischemic study group, i.c. injection of NaCl and exposure to hypoxia after ligation of the left carotid artery (n = 17); or 4) hypoxic-ischemic/LPS study group, i.c. injection of LPS and exposure to hypoxia after ligation of the left carotid artery (n = 19). Seven days later, neonatal brains were assessed for neuronal cell damage. In a second set of experiments, rat pups received an i.c. injection of LPS (5 microg/pup) and were evaluated for tumor necrosis factor-alpha expression by immunohistochemistry. Neuronal cell damage could not be observed in the sham control or in the LPS group. In the hypoxic-ischemic/LPS group, neuronal injury in the cerebral cortex was significantly higher than in animals that were subjected to hypoxia/ischemia after i.c. application of NaCl. Injecting LPS intracisternally caused a marked expression of tumor necrosis factor-alpha in the leptomeninges. Applying LPS intracisternally sensitizes the immature rat brain to a subsequent hypoxic-ischemic insult. | lld:pubmed |
pubmed-article:12621122 | pubmed:language | eng | lld:pubmed |
pubmed-article:12621122 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12621122 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12621122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12621122 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12621122 | pubmed:month | May | lld:pubmed |
pubmed-article:12621122 | pubmed:issn | 0031-3998 | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:LeibStephen... | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:BergerRichard... | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:GarnierYvesY | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:JensenArneA | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:CoumansAudrey... | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:MiddelanisJoh... | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:VaihingerHans... | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:Von... | lld:pubmed |
pubmed-article:12621122 | pubmed:author | pubmed-author:HasaartTom... | lld:pubmed |
pubmed-article:12621122 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12621122 | pubmed:volume | 53 | lld:pubmed |
pubmed-article:12621122 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12621122 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12621122 | pubmed:pagination | 770-5 | lld:pubmed |
pubmed-article:12621122 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:meshHeading | pubmed-meshheading:12621122... | lld:pubmed |
pubmed-article:12621122 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12621122 | pubmed:articleTitle | Intracisternal application of endotoxin enhances the susceptibility to subsequent hypoxic-ischemic brain damage in neonatal rats. | lld:pubmed |
pubmed-article:12621122 | pubmed:affiliation | Department of Obstetrics and Gynecology, University Hospital Maastricht, The Netherlands. | lld:pubmed |
pubmed-article:12621122 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12621122 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |