| pubmed-article:11821008 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11821008 | lifeskim:mentions | umls-concept:C0005854 | lld:lifeskim |
| pubmed-article:11821008 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:11821008 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:11821008 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:11821008 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:11821008 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11821008 | pubmed:dateCreated | 2002-1-31 | lld:pubmed |
| pubmed-article:11821008 | pubmed:abstractText | The first goal of the present study was to determine the effect of tumor necrosis factor-alpha (TNF-alpha) on the permeability of the blood-brain barrier in vivo. The second goal of this study was to investigate cellular pathways responsible for changes in permeability of the blood-brain barrier in response to TNF-alpha. We examined the pial microcirculation in rats using intravital fluorescence microscopy. Permeability of the blood-brain barrier was quantitated by calculating the clearance of fluorescent-labeled dextran (mol. wt=10,000; FITC-dextran-10K) during superfusion with vehicle, tumor necrosis factor (TNF-alpha; 10 ng/ml), TNF-alpha in the presence of an inhibitor of soluble guanylate cyclase (ODQ; 1.0 microM), and TNF-alpha in the presence of an inhibitor of protein tyrosine kinase (genistein; 10 microM). During superfusion with vehicle, clearance of FITC-dextran-10K from pial vessels remained relatively constant during the experimental period. In contrast, superfusion with TNF-alpha markedly increased clearance of FITC-dextran-10K from the cerebral microcirculation. Topical application of ODQ and genistein, significantly inhibited increases in permeability of the blood-brain barrier to FITC-dextran-10K during application of TNF-alpha. Thus, TNF-alpha increases the permeability of the blood-brain barrier to a moderately sized molecule via a mechanism which appears to involve activation of soluble guanylate cyclase and protein tyrosine kinase. In light of evidence suggesting that TNF-alpha production is increased during cerebrovascular trauma, we suggest that the findings of this study may contribute to our understanding of the pathogenesis of disruption of the blood-brain barrier during brain trauma and inflammation. | lld:pubmed |
| pubmed-article:11821008 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11821008 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11821008 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11821008 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11821008 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11821008 | pubmed:issn | 0006-8993 | lld:pubmed |
| pubmed-article:11821008 | pubmed:author | pubmed-author:MayhanWilliam... | lld:pubmed |
| pubmed-article:11821008 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11821008 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11821008 | pubmed:volume | 927 | lld:pubmed |
| pubmed-article:11821008 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11821008 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11821008 | pubmed:pagination | 144-52 | lld:pubmed |
| pubmed-article:11821008 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
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| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
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| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
| pubmed-article:11821008 | pubmed:meshHeading | pubmed-meshheading:11821008... | lld:pubmed |
| pubmed-article:11821008 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11821008 | pubmed:articleTitle | Cellular mechanisms by which tumor necrosis factor-alpha produces disruption of the blood-brain barrier. | lld:pubmed |
| pubmed-article:11821008 | pubmed:affiliation | Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, NE 68198-4575, USA. wgmayhan@unmc.edu | lld:pubmed |
| pubmed-article:11821008 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11821008 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11821008 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11821008 | lld:pubmed |
