摘要目的探讨吸入地塞米松对气道重建和对离体平滑肌增殖作用的影响。方法雄性豚鼠40只，随机分为4组：哮喘组、治疗组、地塞米松组、对照组，每组10只。每组动物连续3个月雾化吸入不同药物后留取病理组织，采用计算机图像分析气道壁厚度。通过对犬气管离体平滑肌细胞培养，测定组胺 (His) 组、血栓素A2组和地塞米松组［3H］ -胸腺嘧啶核苷(［3H］-TdR)的闪烁计数值。结果哮喘组豚鼠气管平滑肌厚度为（90±14）μm ，与对照组（54±7）μm比较，差异有显著性（P<0.01）；治疗组气管平滑肌厚度为（61±11）μm ，与哮喘组比较，差异有显著性（P<0.01）。 His组［3H］-TdR 值为（2 950±205）次/分，与对照组［（613±52 ）次/分］比较，差异有显著性（P<0.01）；地塞米松组［3H］ -TdR值为（1 067±96）次/分，与His组比较差异有显著性（P<0.01）。结论地塞米松能抑制气道平滑肌细胞增殖，早期吸入地塞米松能够有效防治气道重建，对气道无损害作用。

abstractsObjective　To investigate the role of inhaled dexamethasone on airway wall remodeling. Methods　Asthmatic guinea pig models were established， after guinea pigs inhaled ovalbumin and dexamethasone，the thickness of airway wall was determined by contour tracing，using a digitizing pad and microcomputer. To culture airway smooth muscle cells，observe the effect of histamine，thromboxane A2 and dexamethasone on cultured cells. Results　The mean thickness of airway smooth muscle in asthma group was （90±14）μm，greater than that of control （54±7）μm (P<0.01);the airway smooth muscle layer in dexamethasone group (61±11)μm was thinner than that of asthma group (P<0.01). ［3H］-TdR incorporation in histamine group (2 950±205) counts/min was higher，comparing to that of the control （613±52） counts/min (P<0.01); ［3H］-TdR incorporation in dexamethasone group was （1 067±96 ）counts/min，lower than those of histamine group (P<0.01). ConclusionsDexamethasone could prevent airway remodeling，and had no harmful effect on airway wall.