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目的:动态观察运用不同方法建立的两种实验性大鼠慢性阻塞性肺疾病(COPD)模型并比较评估两组模型的特点。方法:分别采用单纯被动吸烟(单一组)和被动吸烟与细菌内毒素(LPS)气管注入的复合方法(复合组)制造大鼠COPD模型,运用HE染色及半定量图像分析法对比研究两组模型肺组织及小支气管的病理形态学改变。结果:建立的COPD大鼠模型均符合人类COPD的病理形态学特点;复合组的气道慢性炎症、重塑改变及气流阻塞情况均较单一组严重;单一组、复合组模型各时间段管壁及平滑肌层均较正常对照组显著增厚(P<0.01),第20天时复合组管壁及平滑肌层均较单一组显著增厚(P<0.01),而第40天及60天时复合组仅管壁较单一组显著增厚(P<0.01)。结论:COPD模型的形成是由于慢性气道炎症的反复刺激引起管壁纤维性增生增厚及平滑肌层增厚,即气道重塑,最终导致气流受限;复合组COPD模型的气道炎症及气道重塑均较单一组COPD模型显著。
OBJECTIVE: To dynamically observe two experimental models of chronic obstructive pulmonary disease (COPD) established by different methods and compare the characteristics of the two models. Methods: The COPD model was made by the combination of passive smoking (single group) and tracheal injection of passive smoking and bacterial endotoxin (LPS) respectively. The model of COPD was made by HE staining and semi-quantitative image analysis Lung and bronchial pathological changes. Results: The established COPD rat model all accorded with the pathomorphological features of human COPD. The chronic airway inflammation, remodeling changes and airflow obstruction in the combined group were more serious than those in the single group. In the single group and composite group, (P <0.01). On the 20th day, the thickness of the wall and the smooth muscle layer in the composite group were significantly thicker than those in the single group (P <0.01), while those on the 40th and 60th days were the same Wall thicker than the single group was significantly (P <0.01). CONCLUSIONS: The COPD model is caused by the repeated stimulation of chronic airway inflammation which leads to thickening of fibrous wall and thickening of smooth muscle layer, ie, airway remodeling, resulting in limited air flow. Airway inflammation in COPD model group and Airway remodeling was more significant than the single COPD model.