Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-8-30
pubmed:abstractText
Nitric oxide (NO) production increases during sepsis and endotoxemia. Inhibition of NO synthase has been suggested as a therapeutic modality in sepsis and endotoxemia, but in recent reports NO synthase inhibition increased mortality rate. The mechanism of this phenomenon is not known. Other studies have shown that high levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6) contribute to death during sepsis and endotoxemia. We tested the effect of NO synthase inhibition on survival in endotoxemic rats and hypothesized that inhibition of NO synthase during endotoxemia increases circulating levels of TNF and IL-6.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0039-6060
pubmed:author
pubmed:issnType
Print
pubmed:volume
116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
332-7; discussion 337-8
pubmed:dateRevised
2010-3-24
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Detrimental effect of nitric oxide synthase inhibition during endotoxemia may be caused by high levels of tumor necrosis factor and interleukin-6.
pubmed:affiliation
Department of Surgery, University of Cincinnati Medical Center, Ohio.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't