{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:58:01Z","timestamp":1790175481700,"version":"4.1.0"},"reference-count":47,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2013,9,1]]},"abstract":"<jats:p>This study was carried out to determine the effect of allergic inflammation on the airway response to increasing airway temperature. Our results showed the following: 1) In Brown-Norway rats actively sensitized by ovalbumin (Ova), isocapnic hyperventilation with humidified warm air (HWA) for 2 min raised tracheal temperature (T<jats:sub>tr<\/jats:sub>) from 33.4 \u00b1 0.6\u00b0C to 40.6 \u00b1 0.1\u00b0C, which induced an immediate and sustained (&gt;10 min) increase in total pulmonary resistance (Rl) from 0.128 \u00b1 0.004 to 0.212 \u00b1 0.013 cmH<jats:sub>2<\/jats:sub>O\u00b7ml<jats:sup>\u22121<\/jats:sup>\u00b7s ( n = 6, P &lt; 0.01). In sharp contrast, the HWA challenge caused the same increase in T<jats:sub>tr<\/jats:sub>but did not generate any increase in Rl in control rats. 2) The increase in Rl in sensitized rats was reproducible when the same HWA challenge was repeated 60\u201390 min later. 3) This bronchoconstrictive effect was temperature dependent: a slightly smaller increase in peak T<jats:sub>tr<\/jats:sub>(39.6 \u00b1 0.2\u00b0C) generated a significant but smaller increase in Rl in sensitized rats. 4) The HWA-induced bronchoconstriction was not generated by the humidity delivered by the HWA challenge alone, because the same water content delivered by saline aerosol at room temperature had no effect. 5) The HWA-evoked increase in Rl in sensitized rats was not blocked by atropine but was completely prevented by pretreatment either with a combination of neurokinin (NK)-1 and NK-2 antagonists or with formoterol, a \u03b2<jats:sub>2<\/jats:sub>agonist, before the HWA challenge. This study showed that increasing airway temperature evoked a pronounced and reversible increase in airway resistance in sensitized rats and that tachykinins released from the vagal bronchopulmonary C-fiber endings were primarily responsible.<\/jats:p>","DOI":"10.1152\/japplphysiol.00491.2013","type":"journal-article","created":{"date-parts":[[2013,7,12]],"date-time":"2013-07-12T04:24:40Z","timestamp":1373603080000},"page":"688-696","source":"Crossref","is-referenced-by-count":15,"title":["Bronchoconstriction induced by increasing airway temperature in ovalbumin-sensitized rats: role of tachykinins"],"prefix":"10.1152","volume":"115","author":[{"given":"Chun-Chun","family":"Hsu","sequence":"first","affiliation":[{"name":"Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan, Republic of China;"},{"name":"Department of Physiology, University of Kentucky Medical Center, Lexington, 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