Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-5-4
pubmed:abstractText
Cardiopulmonary bypass (CPB) is associated with an inflammatory process that leads to lung injury. In this study, we hypothesized that inhaled nitric oxide (INO) possesses the ability to modulate CPB-induced inflammation. Fifteen male pigs were randomly divided into 3 groups: Sham, CPB+LPS (CPB and lipopolysaccharide), and CPB+LPS+INO. INO (20 parts per million) was administered for 24 h after anesthesia. CPB was performed for 90 min, and LPS was infused (1 microg/kg) after CPB. Bronchoalveolar lavage (BAL) fluid and blood were collected at T0 (before CPB), at 4 h, and at 24 h. At 24 h, BAL interleukin-8 (IL-8) levels were not increased as expected in the CPB+LPS group compared with the Sham group, but they were reduced significantly in the CPB+LPS+INO group. Cell hypo reactivity observed in the groups receiving LPS also seemed to downregulate endothelial nitric oxide synthase NOS protein expression relative to the Sham group. Nitrite and nitrate (NOx) concentrations were decreased significantly in the groups without INO. Moreover, animals treated with INO showed higher rates of pulmonary apoptosis compared with their respective controls. These results demonstrate that NOx production is reduced after CPB and that INO acts on the inflammatory process by diminishing neutrophils and their major chemoattractant, IL-8. INO also increases cell apoptosis in the lungs under inflammatory conditions, which may explain, in part, how it resolves pulmonary inflammation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0008-4212
pubmed:author
pubmed:issnType
Print
pubmed:volume
83
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
252-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15870839-Administration, Inhalation, pubmed-meshheading:15870839-Animals, pubmed-meshheading:15870839-Anti-Inflammatory Agents, pubmed-meshheading:15870839-Apoptosis, pubmed-meshheading:15870839-Bronchoalveolar Lavage Fluid, pubmed-meshheading:15870839-Cardiopulmonary Bypass, pubmed-meshheading:15870839-Disease Models, Animal, pubmed-meshheading:15870839-Interleukin-8, pubmed-meshheading:15870839-Lipopolysaccharides, pubmed-meshheading:15870839-Lung, pubmed-meshheading:15870839-Male, pubmed-meshheading:15870839-Neutrophils, pubmed-meshheading:15870839-Nitrates, pubmed-meshheading:15870839-Nitric Oxide, pubmed-meshheading:15870839-Nitric Oxide Synthase, pubmed-meshheading:15870839-Nitric Oxide Synthase Type III, pubmed-meshheading:15870839-Nitrites, pubmed-meshheading:15870839-Pneumonia, pubmed-meshheading:15870839-Swine
pubmed:year
2005
pubmed:articleTitle
The anti-inflammatory effect of inhaled nitric oxide on pulmonary inflammation in a swine model.
pubmed:affiliation
Laboratory of Anesthesia, Department of Anesthesia, Centre hospitalier de l'Université de Montréal-Hôpital Notre-Dame, QC, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't