Linked Life Data

3010781

Source:http://linkedlifedata.com/resource/pubmed/id/3010781

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1986-6-12
pubmed:abstractText
Leukotriene B4 (LTB4) is a metabolite of arachidonic acid that has potent chemotactic activity for polymorphonuclear leukocytes (PMN). Pulmonary oxygen toxicity is considered to be a good model of an acute inflammatory lung injury, and an increase in the number of PMN is found in the lungs acutely injured by hyperoxia. In order to estimate the role of LTB4 responsible for this influx of PMN, we measured the LTB4 by radioimmunoassay in lung lavages of rats exposed to hyperoxia for 60 h. We found that the level of LTB4 in lung lavages in rats exposed to hyperoxia for 60 h increased significantly compared with that in normoxic control rats. At the same time, the marked increase in the number of PMN in lung lavages and the decrease in the activity of NADPH-cytochrome c reductase in lung microsomes were also observed. The administration of AA861, a 5-lipoxygenase inhibitor, reduced not only the increase in LTB4 but also the increase in the number of PMN in lung lavages of rats exposed to hyperoxia for 60 h. Furthermore, treatment with AA861 also protected the decrease in the activity of NADPH-cytochrome c reductase. The effects of AA861 on these parameters were observed in a dose-dependent fashion. In addition, there is a good correlation between the level of LTB4 and the number of PMN in the lavage of rats exposed to hyperoxia for 60 h with or without AA861 administration.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0003-0805
pubmed:author
pubmed:issnType
Print
pubmed:volume
133
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
805-8
pubmed:dateRevised
2010-5-7
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
The role of leukotriene B4 in the genesis of oxygen toxicity in the lung.
pubmed:publicationType
Journal Article