This study investigated whether intermittent hypoxia (IH) induces airway hyperresponsiveness (AHR) and associated with lung inflammation. Male Brown Norway rats were exposed to 14-day IH or room air (RA) for 6 h/day. One day after the last exposure, total lung resistance to various doses of methacholine was measured as an index of bronchoconstrictive responses. Compared with RA controls, methacholine significantly induced an augmented bronchoconstriction in IH-exposed rats. Moreover, IH exposure evoked lung inflammation which was reflected by increased inflammatory cell infiltration, concentrations of interleukin-6 and prostaglandin E₂ in bronchoalveolar lavage fluid, and lung lipid peroxidation. IH-induced AHR and lung inflammation were completely abolished by daily intraperitoneal injection of N-acetylcysteine (an antioxidant) or ibuprofen (a cyclooxygenase inhibitor), but not by apocynin (an inhibitor of NADPH oxidase) or vehicle. In conclusion, AHR and lung inflammation occur after 14-day IH exposure, with endogenous reactive oxygen species and cyclooxygenase metabolites being responsible for these responses.

本研究调查了间歇性缺氧 (IH) 是否会诱发气道高反应性 (AHR) 并与肺部炎症相关。雄性棕色挪威大鼠暴露于 14 天 IH 或室内空气 (RA) 6 小时/天。最后一次暴露后一天，测量对不同剂量乙酰甲胆碱的总肺阻力作为支气管收缩反应的指标。与 RA 对照相比，乙酰甲胆碱显着诱导 IH 暴露大鼠的支气管收缩增强。此外，IH 暴露诱发了肺部炎症，这反映在炎症细胞浸润增加、支气管肺泡灌洗液中白细胞介素 6 和前列腺素 E _{2的浓度以及肺脂质过氧化。}每日腹腔注射N可完全消除 IH 诱导的 AHR 和肺部炎症-乙酰半胱氨酸（一种抗氧化剂）或布洛芬（一种环氧合酶抑制剂），但不是由夹竹桃麻素（一种 NADPH 氧化酶抑制剂）或载体。总之，AHR 和肺部炎症发生在 14 天 IH 暴露后，内源性活性氧和环氧合酶代谢物负责这些反应。