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Lung injury was assessed by the analysis of pulmonary physiology, bronchoalveolar lavage fluid, and morphology. Hydrocarbon exposure to target JP-8 concentrations of 50 mg\/m<jats:sup>3<\/jats:sup>, with saline treatment, was characterized by enhanced respiratory permeability to<jats:sup>99m<\/jats:sup>Tc-labeled diethylenetriaminepentaacetic acid, alveolar macrophage toxicity, and bronchiolar epithelial damage. Mice administered [Sar<jats:sup>9<\/jats:sup>,Met(O<jats:sub>2<\/jats:sub>)<jats:sup>11<\/jats:sup>]substance P, an NK<jats:sub>1<\/jats:sub>-receptor agonist, after each JP-8 exposure had the appearance of normal pulmonary values and tissue morphology. In contrast, endogenous NK<jats:sub>1<\/jats:sub>-receptor antagonism by CP-96345 administration exacerbated JP-8-enhanced permeability, alveolar macrophage toxicity, and bronchiolar epithelial injury. These data indicate that NK<jats:sub>1<\/jats:sub>-receptor activation may have a protective role in preventing the development of hydrocarbon-induced lung injury, possibly through the modulation of bronchiolar epithelial function.<\/jats:p>","DOI":"10.1152\/ajplung.1999.276.2.l229","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T22:52:18Z","timestamp":1514069538000},"page":"L229-L238","source":"Crossref","is-referenced-by-count":5,"title":["NK<sub>1<\/sub>-receptor activation prevents hydrocarbon-induced lung injury in mice"],"prefix":"10.1152","volume":"276","author":[{"given":"Raymond F.","family":"Robledo","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Vermont, Burlington, Vermont 05405-0068; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark L.","family":"Witten","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Arizona, Tucson, Arizona 85724-5073"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0163-7258(90)90065-A"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1996.81.4.1715"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.9.4788"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1990.68.5.1826"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1989.tb08684.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1993.tb13821.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1177\/074823379701300104"},{"issue":"12","key":"B8","first-page":"L584","volume":"268","author":"Ichikawa S.","year":"1995","journal-title":"Am. 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