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Pretreatment with MK-0591 and indomethacin significantly attenuated, but did not abolish, HIB. However, addition of atropine nearly eliminated the residual response. Blockade of eicosanoid metabolism markedly reduced the concentrations of eicosanoids recovered in BALF after hyperventilation. Positive correlations between posthyperventilation BALF prostanoid and epithelial cell concentrations are suggestive of mucosal injury-induced mediator production and release. We conclude that HIB is prevented in the presence of eicosanoid and muscarinic-receptor blockade and that both classes of eicosanoids contribute similarly to the development of HIB.<\/jats:p>","DOI":"10.1152\/jappl.2000.89.5.1949","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:03:06Z","timestamp":1513998186000},"page":"1949-1955","source":"Crossref","is-referenced-by-count":1,"title":["Eicosanoid and muscarinic receptor blockade abolishes hyperventilation-induced bronchoconstriction"],"prefix":"10.1152","volume":"89","author":[{"given":"Arthur N.","family":"Freed","sequence":"first","affiliation":[{"name":"Department of Environmental Health Sciences, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland 21205"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sharron","family":"McCulloch","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, School of 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