| pubmed-article:3277470 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3277470 | lifeskim:mentions | umls-concept:C0699819 | lld:lifeskim |
| pubmed-article:3277470 | lifeskim:mentions | umls-concept:C0036982 | lld:lifeskim |
| pubmed-article:3277470 | lifeskim:mentions | umls-concept:C0243026 | lld:lifeskim |
| pubmed-article:3277470 | lifeskim:mentions | umls-concept:C0449416 | lld:lifeskim |
| pubmed-article:3277470 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:3277470 | pubmed:dateCreated | 1988-3-23 | lld:pubmed |
| pubmed-article:3277470 | pubmed:abstractText | In a model of severe hemorrhagic shock in rats, blood culture findings became positive within 2 to 4 hours of shock. The organisms cultured were primarily gram-negative. To test the hypothesis that the gut was the source of the bacteria, E. coli labeled with carbon-14 oleic acid were fed to rats undergoing hemorrhagic shock. Their plasma was then assayed for carbon-14 activity. Seven of the 14 shocked animals demonstrated increased plasma carbon-14 activity during or after shock. The mortality rate was 100 percent 80 hours postshock, and all animals had E. coli on subsequent blood culture. The seven rats without increased plasma carbon-14 activity had a survival rate of 83 percent postshock. Sham-shocked animals did not exhibit plasma carbon-14 levels greater than the background levels. These data suggest that bacterial translocation occurs during hemorrhagic shock and that the gut is the source of the bacteremia seen during hemorrhagic shock. | lld:pubmed |
| pubmed-article:3277470 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3277470 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3277470 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3277470 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:3277470 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3277470 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3277470 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:3277470 | pubmed:issn | 0002-9610 | lld:pubmed |
| pubmed-article:3277470 | pubmed:author | pubmed-author:SmithSS | lld:pubmed |
| pubmed-article:3277470 | pubmed:author | pubmed-author:RushB FBFJr | lld:pubmed |
| pubmed-article:3277470 | pubmed:author | pubmed-author:LyszT WTW | lld:pubmed |
| pubmed-article:3277470 | pubmed:author | pubmed-author:MachiedoG WGW | lld:pubmed |
| pubmed-article:3277470 | pubmed:author | pubmed-author:SoriA JAJ | lld:pubmed |
| pubmed-article:3277470 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3277470 | pubmed:volume | 155 | lld:pubmed |
| pubmed-article:3277470 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3277470 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3277470 | pubmed:pagination | 187-92 | lld:pubmed |
| pubmed-article:3277470 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:3277470 | pubmed:meshHeading | pubmed-meshheading:3277470-... | lld:pubmed |
| pubmed-article:3277470 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:3277470 | pubmed:articleTitle | The gut as source of sepsis after hemorrhagic shock. | lld:pubmed |
| pubmed-article:3277470 | pubmed:affiliation | Department of Surgery, University of Medicine and Dentistry, New Jersey Medical School, Newark 07103. | lld:pubmed |
| pubmed-article:3277470 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3277470 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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