烟熏加气管内滴入PPE诱发大鼠肺气肿模型

目的肺气肿是一种严重威胁人类健康的常见疾病,为更好地对肺气肿的发病机理和防治措施进行实验研究,建立一种与人类吸烟所致肺气肿相似的实验动物模型.方法采用烟熏1个月后气管内滴入猪胰弹性蛋白酶(porcine pancreaticelastase,PPE)的方法诱发大鼠肺气肿,3个月后行HRCT、肺功能检查和组织病理学观察并与正常对照组比较以评价肺气肿的诱发情况.结果HRCT示实验组周边肺组织肺纹理减少,透光度增强,出现明显的肺气肿的影像学改变.肺功能检查发现实验组肺顺应性和FEV0.3/FVC明显低于正常对照组,吸气阻力和肺总量/体重明显高于正常对照组.组织病理学检查见实验组细支气管黏膜下炎性细胞浸润,肺泡结构紊乱,肺泡壁断裂,肺泡腔融合扩大,与人类慢性阻塞性肺气肿的变化相似.结论烟熏加气管内滴入猪胰弹性蛋白酶成功诱发大鼠的实验性肺气肿,其影像学、肺功能和组织病理学表现均与人类因长期吸烟造成的慢性阻塞性肺气肿相似,是研究人类慢性阻塞性肺气肿的较好实验动物模型.

Induction of emphysema by cigarette inhalation and elastase tracheal instillation in rats

Objectives To establish an experimental animal model which is similar to human pulmonary emphysema caused by cigarette smoking for studying the pathogenesis, prevention and treatment of pulmonary emphysema.Methods The method of cigarette inhalation for 1 month following porcine pancreatic elastase tracheal instillation was used to induce the experimental pulmonary emphysema in Sprague-Dawley rats. 3 months later, high resolution CT, pulmonary function test and pathology were examined to evaluate the rats.Results High resolution CT showed typical pulmonary emphysema image in experimental group. Pulmonary function test showed that lung compliance and perecent of FEV0.3 to FVC of experimental group decreased significantly than that of normal group, inspiratory resistant pressure and the ratio of total lung capacity to body weight increased significantly than that of normal group. The pathological result of experimental group showed chronic bronchitis and emphysema simillar to human emphysema.Conclusion The rat was successfully induced pulmonary emphysema within 3 months by cigarette inhalation for 1 month following porcine pancreatic elastase tracheal instillation. It was a good animal model for studying human pulmonary emphysema.