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There is no clear consensus as to its time\u2010 and inhaled\u2010dose\u2010dependent etiopathologies and associated preventive or therapeutic treatment strategies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Cardiopulmonary function was examined in rats exposed by inhalation to the alveolar irritant phosgene or to the airway irritant chlorine during and following exposure. Terminal measurements focused on hematology, protein extravasation in bronchoalveolar lavage (BAL), and increased lung weight. Noninvasive diagnostic and prognostic endpoints in exhaled breath (carbon dioxide and nitric oxide) were used to detect the clinically occult stage of pulmonary edema.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The first event observed in rats following high but sublethal acute exposure to phosgene was the stimulation of alveolar nociceptive vagal receptors. This afferent stimulation resulted in dramatic changes in cardiopulmonary functions, ventilation: perfusion imbalances, and progressive pulmonary edema and phospholipoproteinosis. Hematology revealed hemoconcentration to be an early marker of pulmonary edema and fibrin as a discriminating endpoint that was positive for the airway irritant chlorine and negative for the alveolar irritant phosgene.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The application of each gas produced typical ALI\/ARDS (acute lung injury\/acute respiratory distress syndrome) characteristics. Phosgene\u2010induced ALI showed evidence of persistent apnea periods, bradycardia, and shifts of vascular fluid from the peripheral to the pulmonary circulation. Carbon dioxide in expired gas was suggestive of increased ventilation dead space and appeared to be a harbinger of progressively developing lung edema. Treatment with the iNOS inhibitor aminoguanidine aerosol by inhalation reduced the severity of phosgene\u2010induced ALI when applied at low dose\u2010rates. Symptomatic treatment regimens were considered inferior to causal modes of treatment.<\/jats:p><\/jats:sec>","DOI":"10.1186\/s40169-017-0149-2","type":"journal-article","created":{"date-parts":[[2017,6,2]],"date-time":"2017-06-02T05:52:23Z","timestamp":1496382743000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Phosgene\u2010induced acute lung injury (ALI): differences from chlorine\u2010induced ALI and attempts to translate toxicology to clinical medicine"],"prefix":"10.1002","volume":"6","author":[{"given":"Wenli","family":"Li","sequence":"first","affiliation":[{"name":"4th Department of Toxicology Fourth Military Medical University No. 169 Changle West Road 710032 Xi\u2019an Shaanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juergen","family":"Pauluhn","sequence":"additional","affiliation":[{"name":"4th Department of Toxicology Fourth Military Medical University No. 169 Changle West Road 710032 Xi\u2019an Shaanxi Province China"},{"name":"Covestro Deutschland AG, Global Phosgene Steering Group K9, 565 51365 Leverkusen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,6,2]]},"reference":[{"key":"e_1_2_13_2_1","unstructured":"United States Army(2005)Potential military chemical\/biological agents and compounds field manual 3\u201311.9. 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