摘要
目的 利用一氧化氮合成前体Ｌ精氨酸（ＬＡｒｇ） 和一氧化氮合酶抑制剂亚硝基Ｌ精氨酸甲酯（ＬＮＡＭＥ）研究内源性一氧化氮在哮喘大鼠气道高反应性中的作用，探讨支气管哮喘的发病机制。方法 用卵白蛋白作为致敏原制备哮喘大鼠模型，建立大鼠离体气管环张力的测定方法，并用ＬＡｒｇ、ＬＮＡＭＥ和ＬＡｒｇ＋ ＬＮＡＭＥ孵育离体气管环，观察气管环乙酰胆碱浓度反应曲线和最大收缩反应的变化，同时观察去上皮对哮喘大鼠气道反应性的影响。结果 哮喘大鼠（１０ 只） 离体气管环经ＬＮＡＭＥ１０５ ｍｏｌ／Ｌ孵育后对乙酰胆碱的最大收缩反应从孵育前（１２４±３９） ｍｇ 上升到（１８７ ±５３） ｍｇ，孵育前、后最大收缩反应比较差异具有显著性（ Ｐ＜ ０．０１），浓度反应曲线上移，而ＬＡｒｇ 可以逆转ＬＮＡＭＥ的作用，单用ＬＡｒｇ ２×１０５ ｍｏｌ／Ｌ和ＬＡｒｇ１０３ ｍｏｌ／Ｌ孵育气管环，对哮喘大鼠气管环的最大收缩反应和浓度反应曲线与对照组比较，差异无显著性（ Ｐ＞ ０．０５） 。去上皮哮喘大鼠气管环的反应性与上皮完整气管环比较差异有显著性（ Ｐ＜ ０．００５） ，而ＬＡｒｇ、ＬＮＡＭＥ＋ ＬＡｒｇ
Objective Nitric oxide (NO) precursor L arginine (L Arg) and NOS inhibitor NG nitro L arginine methyl ester (L NAME) were used to investigate the role of endogenous NO in airway hyperresponsiveness of asthmatic rats. Methods Asthmatic wistar rats were developed by sensitization and challenging with ovalbumin. Airway responsivess to acetylcholine (Ach) was measured in vitro in isolated and perfused rat tracheal rings with or without epithelium after inhibiting or stimulating NO synthesis. Results After asthmatic rat tracheal rings were incubated in vitro with L NAME 10 5 mol/L, the maximal response of tracheal rings to Ach was increased compared with that of the control group. When asthmatic rat tracheal rings were coincubated with L Arginine 2×10 5 mol/L and L NAME 10 5 mol/L, the maximal response was decreased compared with that of the L NAME group. Incubation with higher concentrations of L Arginine did not change asthmatic rat tracheal responsiveness to Ach. Epithelium denuded tracheal rings in the asthmatic rats showed a significant ( P <0.05) upward shift in the Ach concentration response curve; the maximal response was increased compared with the tracheal intact group. In the denuded tracheal rings, L NAME and L Arginine did not influence the shape of the Ach concentration response curve and the maximal response. Conclusiosns Endogenous nitric oxide, a mediator of bronchodilation, is synthesized from L Arginine by NO synthase in asthmatic rats. The epithelium lining airway smooth muscle probably contributes to nitric oxide synthesis. Our finding suggests that the airway in asthmatic rats could not use exogenous L Arginine to synthesize nitric oxide.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
1999年第12期717-719,共3页
Chinese Journal of Tuberculosis and Respiratory Diseases
基金
国家"九五"科技项目基金!资助( 基金编号:969060204)
关键词
一氧化氮
哮喘
气道高反应性
Nitric oxide Airway hyperresponsiveness Asthma
