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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1997-2-10
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pubmed:abstractText |
Acute visceral ischemia and subsequent reperfusion injury, which accompanies the surgical repair of a thoracoabdominal aorta aneurysm, is associated with high rates of morbidity and mortality. The purpose of the present study was to determine whether endogenous tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production contributes to organ dysfunction in animals subjected to visceral ischemia secondary to 30 min of supraceliac aortic occlusion. C57BL6/j mice were treated with either a TNF binding protein (TNF-bp-10 mg/kg) or an anti-IL-1 receptor type 1 antibody (150 micrograms) 2 h prior to 30 min of supraceliac aortic occlusion. An additional group of mice received 30 min of infrarenal aortic occlusion to determine the contribution of lower torso ischemia-reperfusion injury to the changes seen following supraceliac aortic occlusion. Visceral organ ischemia for 30 min produced by supraceliac aortic occlusion followed by 2 h of reperfusion produced measurable TNF-alpha in 38% of untreated mice, but TNF-alpha was undetectable in both sham-operated mice and following infrarenal aortic occlusion. After 2 h of reperfusion, lung myeloperoxidase levels were significantly elevated in the mice experiencing visceral ischemia-reperfusion compared with either a sham operation or infrarenal ischemia-reperfusion (11.6 +/- 1.3 U/g vs. 3.4 +/- .2 U/g and 3.7 +/- 1.0 U/g, respectively, p < .05). Pretreatment with TNF-bp and anti-IL-1 antibody decreased lung neutrophil recruitment (7.2 +/- 1.2 U/g and 4.6 +/- 1.1 U/g) and capillary membrane permeability changes in mice following visceral ischemia-reperfusion. The present study demonstrates that brief (30 min) clinically relevant visceral ischemia produces TNF-alpha and IL-1 dependent lung injury.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aspartate Aminotransferases,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1073-2322
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pubmed:author |
pubmed-author:AbouhamzeA SAS,
pubmed-author:AbouhamzeZZ,
pubmed-author:AuffenburgTT,
pubmed-author:BaumhoferJJ,
pubmed-author:ChizzoniteRR,
pubmed-author:DouglasW GWG,
pubmed-author:EdwardsP DPD,
pubmed-author:HarwardT RTR,
pubmed-author:MartinDD,
pubmed-author:MoldawerL LLL,
pubmed-author:PruittJ HJH,
pubmed-author:SeegerJ MJM,
pubmed-author:WelbornM BMB3rd
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pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
171-6
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8885081-Animals,
pubmed-meshheading:8885081-Aorta, Abdominal,
pubmed-meshheading:8885081-Aspartate Aminotransferases,
pubmed-meshheading:8885081-Capillary Permeability,
pubmed-meshheading:8885081-Female,
pubmed-meshheading:8885081-Interleukin-1,
pubmed-meshheading:8885081-Interleukin-6,
pubmed-meshheading:8885081-Liver,
pubmed-meshheading:8885081-Lung,
pubmed-meshheading:8885081-Lung Injury,
pubmed-meshheading:8885081-Male,
pubmed-meshheading:8885081-Mice,
pubmed-meshheading:8885081-Mice, Inbred C57BL,
pubmed-meshheading:8885081-Peroxidase,
pubmed-meshheading:8885081-Reperfusion Injury,
pubmed-meshheading:8885081-Time Factors,
pubmed-meshheading:8885081-Tumor Necrosis Factor-alpha,
pubmed-meshheading:8885081-Vascular Surgical Procedures
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pubmed:year |
1996
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pubmed:articleTitle |
Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse.
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pubmed:affiliation |
Department of Surgery, University of Florida College of Medicine, Gainesville 32610, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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