| pubmed-article:7528979 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7528979 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:7528979 | lifeskim:mentions | umls-concept:C0205054 | lld:lifeskim |
| pubmed-article:7528979 | lifeskim:mentions | umls-concept:C0376618 | lld:lifeskim |
| pubmed-article:7528979 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:7528979 | pubmed:issue | 6 Pt 1 | lld:pubmed |
| pubmed-article:7528979 | pubmed:dateCreated | 1995-1-31 | lld:pubmed |
| pubmed-article:7528979 | pubmed:abstractText | Nitric oxide (NO) has been reported to have a protective function in attenuating hepatic injury during endotoxemia or sepsis. As a result, the role of NO in attenuating the hepatic microcirculatory alterations associated with endotoxemia was investigated in mice by in vivo microscopy. The livers were examined 2 h after intravenous injection of Escherichia coli 0111:B4 lipopolysaccharide (LPS) alone or in combination with inhibitors of the synthesis of NO, NG-nitro-L-arginine methyl ester or NG-monomethyl-L-arginine. In the animals treated with the combination of NO synthase inhibitors and LPS, leukocyte adherence was increased threefold above that in animals treated with LPS alone. This was accompanied by a 33% reduction in sinusoidal blood flow. Simultaneous administration of L-arginine, but not D-arginine, eliminated these microcirculatory disturbances. The results demonstrate that inhibition of LPS-stimulated NO production results in an early hepatic microvascular inflammatory response to a dose of endotoxin which by itself is scarcely inflammatory. This suggests that NO plays a significant role in stabilizing the hepatic microcirculation during endotoxemia, thereby helping to protect the liver from ischemia and leukocyte-induced oxidative injury. | lld:pubmed |
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| pubmed-article:7528979 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7528979 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7528979 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7528979 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7528979 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:7528979 | pubmed:author | pubmed-author:McDonnellDD | lld:pubmed |
| pubmed-article:7528979 | pubmed:author | pubmed-author:McCuskeyR SRS | lld:pubmed |
| pubmed-article:7528979 | pubmed:author | pubmed-author:NishideFF | lld:pubmed |
| pubmed-article:7528979 | pubmed:author | pubmed-author:FooE LEL | lld:pubmed |
| pubmed-article:7528979 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7528979 | pubmed:volume | 267 | lld:pubmed |
| pubmed-article:7528979 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7528979 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7528979 | pubmed:pagination | G1135-41 | lld:pubmed |
| pubmed-article:7528979 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:7528979 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7528979 | pubmed:articleTitle | Protective role of NO in hepatic microcirculatory dysfunction during endotoxemia. | lld:pubmed |
| pubmed-article:7528979 | pubmed:affiliation | Department of Anatomy, College of Medicine, University of Arizona, Tucson 85724. | lld:pubmed |
| pubmed-article:7528979 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7528979 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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