pubmed-article:9468170 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9468170 | lifeskim:mentions | umls-concept:C0032285 | lld:lifeskim |
pubmed-article:9468170 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
pubmed-article:9468170 | lifeskim:mentions | umls-concept:C0243026 | lld:lifeskim |
pubmed-article:9468170 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:9468170 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:9468170 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
pubmed-article:9468170 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:9468170 | pubmed:dateCreated | 1998-2-26 | lld:pubmed |
pubmed-article:9468170 | pubmed:abstractText | Increases in exhaled nitric oxide have been demonstrated to originate from the lungs of rats after septic lung injury. The aim of this study was to investigate whether treatment with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) would prevent lipopolysaccharide (LPS)-induced increases in exhaled nitric oxide and whether this would have an effect on septic lung inflammation. | lld:pubmed |
pubmed-article:9468170 | pubmed:language | eng | lld:pubmed |
pubmed-article:9468170 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9468170 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:9468170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9468170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9468170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9468170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9468170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9468170 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9468170 | pubmed:month | Feb | lld:pubmed |
pubmed-article:9468170 | pubmed:issn | 0090-3493 | lld:pubmed |
pubmed-article:9468170 | pubmed:author | pubmed-author:VolgyesiGG | lld:pubmed |
pubmed-article:9468170 | pubmed:author | pubmed-author:ValenzaFF | lld:pubmed |
pubmed-article:9468170 | pubmed:author | pubmed-author:MullenJ BJB | lld:pubmed |
pubmed-article:9468170 | pubmed:author | pubmed-author:SlutskyA SAS | lld:pubmed |
pubmed-article:9468170 | pubmed:author | pubmed-author:StewartT ETE | lld:pubmed |
pubmed-article:9468170 | pubmed:author | pubmed-author:AaronS DSD | lld:pubmed |
pubmed-article:9468170 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9468170 | pubmed:volume | 26 | lld:pubmed |
pubmed-article:9468170 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9468170 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9468170 | pubmed:pagination | 309-14 | lld:pubmed |
pubmed-article:9468170 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:9468170 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9468170 | pubmed:articleTitle | Inhibition of exhaled nitric oxide production during sepsis does not prevent lung inflammation. | lld:pubmed |
pubmed-article:9468170 | pubmed:affiliation | Department of Medicine, University of Ottawa, ON, Canada. | lld:pubmed |
pubmed-article:9468170 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9468170 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:9468170 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |