Linked Life Data

2543658

Source:http://linkedlifedata.com/resource/pubmed/id/2543658

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1989-7-18
pubmed:abstractText
The sulfidopeptide leukotrienes are bronchoconstrictive lipid mediators thought to have an important role in the pathophysiology of asthma. The objective of this study was to determine if treatment with a leukotriene receptor antagonist and 5-lipoxygenase inhibitors could diminish acrolein-induced bronchial hyperresponsiveness and to determine whether leukotriene (LT) C4 generation is augmented by acrolein exposure. Guinea pigs (groups of 6-7) were exposed to 1.3 ppm acrolein for 2 h and bronchial responsiveness to intravenous acetylcholine determined twice before, and once 1, 2, 6, and 24 h after exposure. Immediately after acrolein exposure (5 min) specific total airway resistance (sRt) increased from 0.86 +/- 0.01 to 1.29 +/- 0.07 ml.cmH2O.ml-1.s. Within 1 h after exposure, the effective dose of acetylcholine sufficient to double sRt (ED200) decreased from 114.0 +/- 6.6 to 58.5 +/- 6.5 micrograms.kg-1.min-1. Bronchial hyperresponsiveness became maximal at 2 h with ED200 = 44.7 +/- 4.2 and persisted for up to 24 h after exposure (24 h ED200 = 60.2 +/- 11.6 micrograms.kg-1.min). A LTC4/LTD4 receptor antagonist, L-649,923 (10 mg/kg iv), and two putative inhibitors of 5-lipoxygenase, L-651,392 (10 mg/kg po) and U-60,257 (5 mg/kg i.v.), diminished the immediate bronchoconstriction and markedly inhibited bronchial hyperresponsiveness. Analysis of bronchoalveolar lavage fluid obtained from guinea pigs after acrolein exposure revealed a significant increase in immunoreactive LTC4 concentrations (control LTC4 = 8.8 +/- 0.3, n = 7; exposed LTC4 = 15.9 +/- 2.4 pg/ml, n = 6). Treatment with L-651,392 inhibited this response (acrolein exposed = 9.4 +/- 2.4 pg/ml, n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/4-bromo-2,7-dimethoxy-3H-phenothiazi..., http://linkedlifedata.com/resource/pubmed/chemical/Acrolein, http://linkedlifedata.com/resource/pubmed/chemical/Aldehydes, http://linkedlifedata.com/resource/pubmed/chemical/Arachidonate Lipoxygenases, http://linkedlifedata.com/resource/pubmed/chemical/Epoprostenol, http://linkedlifedata.com/resource/pubmed/chemical/L 649923, http://linkedlifedata.com/resource/pubmed/chemical/Leukotrienes, http://linkedlifedata.com/resource/pubmed/chemical/Lipoxygenase Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Phenothiazines, http://linkedlifedata.com/resource/pubmed/chemical/Phenylbutyrates, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Leukotriene, http://linkedlifedata.com/resource/pubmed/chemical/SRS-A, http://linkedlifedata.com/resource/pubmed/chemical/piriprost
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1838-45
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Sulfidopeptide leukotrienes mediate acrolein-induced bronchial hyperresponsiveness.
pubmed:affiliation
Department of Environmental Health, University of Cincinnati Medical Center, Ohio 45267-0182.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.