| pubmed-article:7889268 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C1801960 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C0264995 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C0036974 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C0680727 | lld:lifeskim |
| pubmed-article:7889268 | lifeskim:mentions | umls-concept:C0679823 | lld:lifeskim |
| pubmed-article:7889268 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:7889268 | pubmed:dateCreated | 1995-4-19 | lld:pubmed |
| pubmed-article:7889268 | pubmed:abstractText | 1. Splanchnic artery occlusion (SAO) shock is characterized by irreversible circulatory failure. Tumour necrosis factor (TNF-alpha) may affect the L-arginine/nitric oxide (NO) pathway, thus contributing to the cardiovascular derangements of circulatory shock. 2. We investigated the contribution of both TNF-alpha and the L-arginine/nitric oxide pathway to the vascular dysfunction of SAO shock. Anaesthetized rats, subjected to total occlusion of the superior mesenteric artery and the coeliac trunk for 45 min developed a severe shock state (SAO shock) resulting in a fatal outcome within 75-90 min after the release of occlusion. Sham operated animals were used as controls. SAO shocked rats had also a marked hypotension and enhanced macrophage and serum levels of TNF-alpha. Furthermore, aortic rings from shocked rats showed a marked hyporeactivity to phenylephrine (PE 1 nM-10 microM) and reduced responsiveness to acetylcholine (ACh 10 nM-10 microM). Endothelium-denuded aortic rings had also a marked hyporeactivity to phenylephrine, which was restored to control values by in vitro administration of NG nitro-L-arginine-methyl ester (L-NAME 10 microM). 3. In vivo administration of cloricromene (2 mg kg-1, i.v.), an inhibitor of TNF-alpha biosynthesis, increased survival, enhanced mean arterial blood pressure and reduced macrophage and serum levels of TNF-alpha. Furthermore, aortic rings from shocked rats treated with cloricromene exhibited a greater contractile response to phenylephrine and improved responsiveness to ACh when compared to aortic rings from vehicle-treated SAO shocked rats. 4. Our results suggest that TNF-alpha alters both endothelial and muscular L-arginine/nitric oxide pathways which in turn produce vascular dysfunction in SAO shock. | lld:pubmed |
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| pubmed-article:7889268 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7889268 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7889268 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7889268 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7889268 | pubmed:issn | 0007-1188 | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:SquadritoGG | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:SaittaAA | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:CanalePP | lld:pubmed |
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| pubmed-article:7889268 | pubmed:author | pubmed-author:SquadritoFF | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:CampoG MGM | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:ZingarelliBB | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:IoculanoMM | lld:pubmed |
| pubmed-article:7889268 | pubmed:author | pubmed-author:AmmendoliaLL | lld:pubmed |
| pubmed-article:7889268 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7889268 | pubmed:volume | 113 | lld:pubmed |
| pubmed-article:7889268 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7889268 | pubmed:authorsComplete | N | lld:pubmed |
| pubmed-article:7889268 | pubmed:pagination | 1153-8 | lld:pubmed |
| pubmed-article:7889268 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7889268 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7889268 | pubmed:articleTitle | Participation of tumour necrosis factor and nitric oxide in the mediation of vascular dysfunction in splanchnic artery occlusion shock. | lld:pubmed |
| pubmed-article:7889268 | pubmed:affiliation | Institute of Pharmacology, School of Medicine, University of Messina, Italy. | lld:pubmed |
| pubmed-article:7889268 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7889268 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:7889268 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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