{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:54:09Z","timestamp":1773420849372,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1995,3,1]]},"abstract":"<jats:p> This study examines the morphological and physiological changes that occur in canine peripheral airways after hyperpnea with dry air. Peripheral airways were exposed to a 5-min 2,000 ml\/min dry air challenge (DAC) at 24, 6, 2, or 1 h before or 60 s after (0 h) the injection of colloidal carbon. After recording the dry air-induced increase in peripheral airway resistance, the lungs were removed and prepared for morphometric analysis (n = 5). Light microscopy revealed that 50% of the airway perimeter appeared damaged at 0, 1, and 2 h after DAC, and repair was evident 6\u201324 h after the challenge. The average goblet-to-ciliated cell ratio decreased from 0.34 before DAC to 0.15 after DAC and recovered within 24 h. Dry air-induced bronchovascular leakage occurred immediately after DAC and persisted for &gt; or = 24 h. DAC decreased mast cell number only in regions where the mucosa was damaged, and this decrease was inversely correlated with bronchovascular leakage. Finally, leukocyte infiltration was evident 1\u20132 h after DAC and continued throughout the 24-h period. We conclude that hyperpnea with dry air causes mucosal injury, inflammation, and microvascular leakage and that these dry air-induced effects persist for &gt; or = 24 h after DAC. <\/jats:p>","DOI":"10.1152\/jappl.1995.78.3.1043","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T11:28:51Z","timestamp":1513942131000},"page":"1043-1051","source":"Crossref","is-referenced-by-count":50,"title":["Hyperpnea with dry air causes time-dependent alterations in mucosal morphology and bronchovascular permeability"],"prefix":"10.1152","volume":"78","author":[{"given":"C.","family":"Omori","sequence":"first","affiliation":[{"name":"Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B. H.","family":"Schofield","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W.","family":"Mitzner","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. N.","family":"Freed","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["Journal of Applied Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jappl.1995.78.3.1043","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:02:24Z","timestamp":1567965744000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1995.78.3.1043"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1995,3,1]]}},"alternative-id":["10.1152\/jappl.1995.78.3.1043"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1995.78.3.1043","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,3,1]]}}}