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目的 探讨低压缺氧治疗哮喘的机制。方法：采用卵蛋白致敏和激发制成豚鼠哮喘模型，比较正常组、诱发哮喘发作后２４小时（发作组）、未经任何治疗哮喘豚鼠（对照组）以及低压缺氧治疗哮喘豚鼠（治疗组）的血浆皮质醇、支气管肺泡灌洗液（ＢＡＬＦ）中嗜酸性粒细胞（ＥＯＳ）和低密度嗜酸性粒细胞（ＨＥＯ）以及肺组织病理学变化。结果（１）皮质醇水平发作组较正常组显著升高（Ｐ＜０．０１），对照组较正常组明显下降（Ｐ＜０．０１），治疗组较对照组显著升高（Ｐ＜０．０１），与正常温无显著差异（Ｐ＞０．０５）。（２）ＢＡＬＦ中ＥＯＳ和ＨＥＯ变化：发作组较正常组明显升高（Ｐ ＜０．０１．治疗组较对照组明显减少（ Ｐ＜０． ０５），治疗组与正常组无显著差异（ Ｐ＞０． ０５）。（３）肺组织病理学变化；治疗组较对照组明显好转，ＥＯＳ浸润减小，肺泡膈间质水肿基本消失，Ⅱ型肺泡上皮增生。结论低压缺氧治疗哮喘豚鼠后血浆皮质醇水平升高，ＢＡＬＦ中ＥＯＳ和ＨＥＯ数目减少，可能是低压缺氧治疗哮喘的机制。
Objective To investigate the mechanism of hypobaric hypoxia in the treatment of asthma. Methods: Guinea pig asthma model was made by sensitization and challenge with ovalbumin. Compared with normal group, asthma was induced in guinea pigs (control group) and asthma guinea pigs (untreated group) by 24 h after onset of asthma (control group) Plasma cortisol, eosinophils (EOS) and low density eosinophils (HEO) in bronchoalveolar lavage fluid (BALF) as well as histopathological changes in lung tissue. Results (1) The level of cortisol in the attack group was significantly higher than that in the normal group (P <0.01), and the level in the control group was significantly lower than that in the normal group (P <0.01) .01), no significant difference with normal temperature (P> 0.05). (2) The changes of EOS and HEO in BALF: The onset group was significantly higher than the normal group (P <0.01. The treatment group was significantly lower than the control group (P <0.05), and the treatment group and the normal group had no significant difference (P > 0.05). (3) Pathological changes of lung tissue: The treatment group was better than the control group, the EOS infiltration was reduced, the alveolar interstitial edema disappeared, and the type II alveolar epithelial hyperplasia was found.Conclusion Hypobaric hypoxia treatment of asthmatic guinea pigs Elevated plasma cortisol levels and a decrease in the number of EOS and HEO in BALF may be the mechanism of hypobaric hypoxia in the treatment of asthma.