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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1995-4-19
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1292885,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1375677,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1376822,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1423915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1468489,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1573976,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1601052,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1689048,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1700903,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1701990,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1702067,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1720542,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-1852778,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2040364,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2113184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2305894,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2542186,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2555881,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2766481,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-2785770,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-3345594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-3390182,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-3495737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-6997383,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-7441497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-7678341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-8184928,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7889268-8396037
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0007-1188
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
113
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pubmed:owner |
NLM
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pubmed:authorsComplete |
N
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pubmed:pagination |
1153-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7889268-Acetylcholine,
pubmed-meshheading:7889268-Animals,
pubmed-meshheading:7889268-Aorta, Thoracic,
pubmed-meshheading:7889268-Blood Pressure,
pubmed-meshheading:7889268-Chromonar,
pubmed-meshheading:7889268-Cyclic AMP,
pubmed-meshheading:7889268-Male,
pubmed-meshheading:7889268-Muscle, Smooth, Vascular,
pubmed-meshheading:7889268-Muscle Contraction,
pubmed-meshheading:7889268-Muscle Relaxation,
pubmed-meshheading:7889268-Nitric Oxide,
pubmed-meshheading:7889268-Phenylephrine,
pubmed-meshheading:7889268-Rats,
pubmed-meshheading:7889268-Rats, Sprague-Dawley,
pubmed-meshheading:7889268-Shock,
pubmed-meshheading:7889268-Splanchnic Circulation,
pubmed-meshheading:7889268-Tumor Necrosis Factor-alpha
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pubmed:year |
1994
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pubmed:articleTitle |
Participation of tumour necrosis factor and nitric oxide in the mediation of vascular dysfunction in splanchnic artery occlusion shock.
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pubmed:affiliation |
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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