Source:http://linkedlifedata.com/resource/pubmed/id/11734449
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10 Pt 1
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| pubmed:dateCreated |
2001-12-5
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| pubmed:abstractText |
Oxidant-mediated reperfusion injury of the gut is a major contributor of the systemic inflammatory response in hemorrhagic shock. Recent studies have suggested that heme-oxygenase-1 (HO-1) represents an endogenous protective mechanism against oxidant stress. We assessed whether HO-1 induction modulates the synthesis of tumor necrosis factor-alpha (TNF-alpha) in hemorrhagic shock. In rats submitted to hemorrhagic shock, pretreatment with hemoglobin (Hb) increased HO-1 mRNA expression in macrophages. This increased expression was associated with a decreased expression of TNF-alpha mRNA, as well as decreased plasma concentrations of TNF-alpha. These effects of Hb were reduced by the HO-1 inhibitor tin-protoporphyrin (Sn-PP 20 micromol/kg), while Sn-PP had no effect in the absence of Hb. In parallel, Hb pretreatment reduced pulmonary edema, vascular injury, and increased mesenteric blood flow, and these effects were reduced by Sn-PP. Thus, induction of HO-1 is protective in hemorrhagic shock, possibly through its antioxidant properties. Interventions that induce HO-1 may be beneficial in the treatment of shock states, leading to a reduced systemic inflammatory response.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1073-449X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
164
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1933-8
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11734449-Animals,
pubmed-meshheading:11734449-Disease Models, Animal,
pubmed-meshheading:11734449-Drug Evaluation, Preclinical,
pubmed-meshheading:11734449-Fluid Therapy,
pubmed-meshheading:11734449-Gene Expression Regulation,
pubmed-meshheading:11734449-Heme Oxygenase (Decyclizing),
pubmed-meshheading:11734449-Hemodynamics,
pubmed-meshheading:11734449-Inflammation,
pubmed-meshheading:11734449-Intestines,
pubmed-meshheading:11734449-Macrophages, Peritoneal,
pubmed-meshheading:11734449-Male,
pubmed-meshheading:11734449-RNA, Messenger,
pubmed-meshheading:11734449-Rats,
pubmed-meshheading:11734449-Rats, Wistar,
pubmed-meshheading:11734449-Reperfusion Injury,
pubmed-meshheading:11734449-Resuscitation,
pubmed-meshheading:11734449-Shock, Hemorrhagic,
pubmed-meshheading:11734449-Splanchnic Circulation,
pubmed-meshheading:11734449-Systemic Inflammatory Response Syndrome,
pubmed-meshheading:11734449-Tumor Necrosis Factor-alpha
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| pubmed:year |
2001
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| pubmed:articleTitle |
Induction of heme-oxygenase-1 prevents the systemic responses to hemorrhagic shock.
|
| pubmed:affiliation |
INSERM E9920, IFRMP and Service de Réanimation Médicale, Rouen University Hospital, France. fabienne.tamion@chu-rouen.fr
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| pubmed:publicationType |
Journal Article
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