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目的通过实验性哮喘豚鼠的肺组织、支气管肺泡灌洗液 (BALF)和血浆中的血管紧张素系统 (ATs)的变化，探讨 ATs与哮喘发病的关系以及吸入糖皮质激素对其的作用。方法将 27只豚鼠随机分为哮喘组 (向豚鼠腹腔内注射含有卵清蛋白的致敏剂致敏， 3周后，经超声雾化吸入 1％卵清蛋白气雾剂诱发豚鼠哮喘 )、激素组 (吸入卵清蛋白前，预先吸入 40 mg/dl地塞米松 20 min，余同哮喘组 )和对照组 (以等量生理盐水代替卵清蛋白 )，每组 9只，分别检测它们的肺切碎活组织、 BALF和血浆中的血管紧张素 I(ATⅠ )、血管紧张素Ⅱ (ATⅡ )水平和血清血管紧张素转换酶 (ACE)的活性。结果哮喘组肺切碎活组织、 BALF中 ATⅠ、 ATⅡ水平及 ACE活性均较对照组显著升高 (P< 0 01)；激素组显示糖皮质激素可使 BALF中 ATs各成分降低，但三组间血浆 ATⅠ、 ATⅡ水平和血清 ACE活性比较，差异均无显著性。结论肺组织可能存在局部 ATs，该系统在哮喘急性发作时被活化，并参与哮喘发病的病理生理过程。 ATⅡ由局部产生，但可能只在局部起作用。吸入糖皮质激素可抑制 ATs活性而起到保护肺、抑制哮喘发作的作用。
Objective To investigate the relationship between ATs and asthma and the effects of inhaled glucocorticoids on the changes of lung tissue, bronchoalveolar lavage fluid (BALF) and plasma angiotensin system (ATs) in experimental asthmatic guinea pigs. Methods Twenty-seven guinea pigs were randomly divided into asthma group (sensitized with ovalbumin to guinea pigs by intraperitoneal injection), guinea pig asthma induced by aerosol inhalation of 1% ovalbumin aerosol after 3 weeks, hormone Group (pre-inhaled ovalbumin, pre-inhalation of dexamethasone 40 mg / dl 20 min, the rest with the asthma group) and the control group (with an equal volume of normal saline instead of ovalbumin), each group of nine, were detected in their lungs The activity of ATⅠ, ATⅡ and serum angiotensin converting enzyme (ACE) in living tissue, BALF and plasma were shredded. Results The levels of ATⅠ, ATⅡ and ACE activity in lung tissue and BALF in asthmatic group were significantly higher than those in control group (P <0.01). The glucocorticoid group showed that glucocorticoid decreased the content of ATs in BALF, Plasma ATⅠ, ATⅡ levels and serum ACE activity between the two groups showed no significant difference. Conclusion There may be local ATs in lung tissue. The system is activated during acute asthma attack and participates in the pathophysiological process of asthma. AT II is produced locally, but may only work locally. Inhaled glucocorticoids can inhibit the ATs activity and play a protective lung, inhibit the role of asthma attacks.