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出 处:《重庆医学》1999年第1期7-10,共4页Chongqing medicine
摘 要: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 explore the mechanism for the therapeutic effects of hypobaric hypoxia on asthmatic gumea pigs. Methods: After the model of asthma was established by ovalbumin (OA ) challenge in OA sensitized guinea pigs. the animals was randomized into the asthmatic group (AG ), the non-treated group (NTG) and hypobaric hypoxia- treated group (HHTG). The level of plasma cortisol and the number of eosinophils (EOS ) and hypodense cosinophils (HEO) in bronchoalveolar lavage fluid (BALF) were determined. The pulmonary pathological changes were observed with optical microscope and electron microscope. Results: (1)Tile level of plasma cortisol was significantly higher in AG than in normal control(NC) (P <0. 01). But the level of plasma cortisol was sighificantly lower in NTG than in HHTG (P <0.01). (2)The number of EOS and HEO was highest in AG. The number of EOS and HEO was signifieantly lower in HHTG(P <0. 05) than in NTG. (3)Infiltration of EOS in the alveolar septum,evacuation of lamellar body and in terstitial edema of the alveolar septum were seen in AG and NTG while all these were improved in HHTG and the alveo lar type II cell proliferated. Conclusion : After the treatment with hypobaric hypoxia,the level of plasma cortisol and the number of EOS and HEO in BALF markedly decreased. All these may be the mechanism for the therapeutic effects of hypobaric hypoxia on asthma.
关 键 词:低压缺氧治疗 哮喘 皮质醇 嗜酸性粒细胞 BALF
分 类 号:R562.250.5[医药卫生—呼吸系统]
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