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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1995-7-13
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pubmed:abstractText |
The influence of pentoxifylline (PTX) on mortality and some important mediators was studied in a model of cecal perforation with fulminant intra-abdominal sepsis in rats. Cumulative mortality was registered in three groups of animals: untreated sepsis (n = 36), sepsis + PTX 20 mg/kg/24 h (n = 24), and sepsis + PTX 80 mg/kg/24 h (n = 24). PTX therapy was started at sepsis induction or after 4 h, and mortality was reduced from 89% in untreated sepsis to 60-66% in the PTX groups. Levels of sepsis mediators were studied in two groups: untreated sepsis and sepsis + PTX 40 mg/kg started 1 h after sepsis induction. In both groups 6-10 animals were sacrificed at 4 and 8 h to measure blood levels of bacteria, endotoxin, tumor necrosis factor (TNF), interleukin-6 (IL-6), endothelin-1, lactate, neutrophils, and packed cell volume. Cecal perforation gave high levels of bacteria, endotoxin, TNF, IL-6, and endothelin-1, leading to dehydration, lactacidosis, neutropenia, and death. Treatment with PTX did not modify dehydration, neutropenia, or concentrations of bacteria and endotoxin. Release of endothelin-1 was delayed, TNF burst was nearly abolished, and levels of IL-6 and lactate were substantially suppressed. In summary, PTX improves survival and reduces blood concentrations of TNF, IL-6, lactate, and endothelin-1 in fulminant intra-abdominal sepsis in rats. The primary effect of PTX in this sequence is probably reduction of TNF.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Endothelins,
http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lactates,
http://linkedlifedata.com/resource/pubmed/chemical/Lactic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Pentoxifylline,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1073-2322
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
210-5
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7773801-Abdomen,
pubmed-meshheading:7773801-Animals,
pubmed-meshheading:7773801-Cecal Diseases,
pubmed-meshheading:7773801-Disease Models, Animal,
pubmed-meshheading:7773801-Endothelins,
pubmed-meshheading:7773801-Endotoxins,
pubmed-meshheading:7773801-Interleukin-6,
pubmed-meshheading:7773801-Intestinal Perforation,
pubmed-meshheading:7773801-Lactates,
pubmed-meshheading:7773801-Lactic Acid,
pubmed-meshheading:7773801-Male,
pubmed-meshheading:7773801-Mice,
pubmed-meshheading:7773801-Pentoxifylline,
pubmed-meshheading:7773801-Rats,
pubmed-meshheading:7773801-Rats, Wistar,
pubmed-meshheading:7773801-Sepsis,
pubmed-meshheading:7773801-Shock, Septic,
pubmed-meshheading:7773801-Survival Rate,
pubmed-meshheading:7773801-Time Factors,
pubmed-meshheading:7773801-Tumor Necrosis Factor-alpha
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pubmed:year |
1995
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pubmed:articleTitle |
Pentoxifylline improves survival and reduces tumor necrosis factor, interleukin-6, and endothelin-1 in fulminant intra-abdominal sepsis in rats.
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pubmed:affiliation |
Department of Surgery, Norwegian Radium Hospital, Oslo.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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