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为探讨内源性一氧化氮 (NO)对支气管哮喘 (哮喘 )气道炎症嗜酸性粒细胞 (EOS)的影响 ,用鸡卵清蛋白 (OVA)腹腔致敏和反复超声雾化吸入 ,刺激复制大鼠过敏性气道炎症模型 .结果表明 ,正常大鼠 (6只 )支气管粘膜下未见嗜酸性粒细胞 ,而致敏大鼠 (6只 )支气管粘膜下EOS〔2 5± 5 (平均每视野计数 ,下同 )〕增多 .NO合成抑制剂 (NOS ,4只 )可使致敏大鼠气道EOS(13± 5 ,P <0 0 5 )减少 ,而NO合成前体则有使EOS进一步增多的趋势 ,提示一定水平的内源性NO与大鼠过敏性气道炎症嗜酸性粒细胞有关
In order to investigate the effect of endogenous nitric oxide (NO) on airway inflammatory eosinophils (EOS) in bronchial asthma (asthma), the mice were sensitized by intraperitoneal hypersensitivity with ovalbumin (OVA) Rat allergic airway inflammation model.The results showed that eosinophils were not found in bronchial submucosa of normal rats (6 rats), while bronchial mucosal EOS 〔2 5 ± 5 (average per field of vision (NOS, 4) could decrease the airway EOS (13 ± 5, P <0 05) in sensitized rats, while the NO synthesis precursors could further decrease the EOS Increased trend, suggesting that a certain level of endogenous NO and allergic airway inflammation eosinophils in rats