Hsu Chun-Chun, Tapia Reyno J, Lee Lu-Yuan
Department of Physiology, University of Kentucky Medical Center, 800 Rose St., MS511A, Lexington, KY 40536-0298, USA.
Department of Physiology, University of Kentucky Medical Center, 800 Rose St., MS511A, Lexington, KY 40536-0298, USA.
Respir Physiol Neurobiol. 2015 Jul;212-214:46-9. doi: 10.1016/j.resp.2015.04.002. Epub 2015 Apr 9.
This study was carried out to determine whether hyperventilation of humidified warm air (HWA) induced airway extravasation in ovalbumin (Ova)-sensitized rats. Our results showed: (1) After isocapnic hyperventilation with HWA for 2 min, tracheal temperature (Ttr) was increased to 40.3°C, and the Evans blue contents in major airways and lung tissue were elevated to 651% and 707%, respectively, of that after hyperventilation with humidified room air in Ova-sensitized rats; this striking effect of HWA was absent in control rats. (2) The HWA-induced increase in Evans blue content in sensitized rats was completely prevented by a pretreatment with either L-732138, a selective antagonist of neurokinin type 1 (NK-1) receptor, or formoterol, a selective agonist of β2 adrenoceptor. This study demonstrated that an increase in airway temperature induced protein extravasation in the major airways and lung tissue of sensitized rats, and an activation of the NK-1 receptor by tachykinins released from bronchopulmonary C-fiber nerve endings was primarily responsible.
本研究旨在确定在卵清蛋白（Ova）致敏大鼠中，湿化暖空气（HWA）过度通气是否会引起气道渗出。我们的结果显示：（1）在卵清蛋白致敏大鼠中，用HWA进行等容过度通气2分钟后，气管温度（Ttr）升至40.3°C，主要气道和肺组织中的伊文思蓝含量分别升至用湿化室内空气过度通气后的651%和707%；在对照大鼠中未观察到HWA的这种显著作用。（2）用神经激肽1型（NK-1）受体选择性拮抗剂L-732138或β2肾上腺素能受体选择性激动剂福莫特罗预处理，可完全阻止HWA诱导的致敏大鼠伊文思蓝含量增加。本研究表明，气道温度升高会导致致敏大鼠主要气道和肺组织中的蛋白质渗出，支气管肺C纤维神经末梢释放的速激肽激活NK-1受体起主要作用。
