【摘要】 目的　探讨细菌在慢性阻塞性肺疾病（ＣＯＰＤ） 发病中的作用。方法　将Ｗｉｓｔａｒ 大鼠１０５只分为３ 组，每组３５ 只。应用多次经鼻腔注入肺炎克雷伯杆菌菌液或肺炎链球菌菌液的呼吸道感染方法试制ＣＯＰＤ大鼠模型，观察其气道形态改变，检测动脉血氧分压（ＰａＯ２） 、血二氧化碳分压（ＰａＣＯ２）和右心室收缩压（ＲＶＳＰ） 。结果　肺炎克雷伯杆菌感染组第１ 周起和肺炎链球菌感染组第４ 周起，大鼠各级细支气管上皮细胞明显损伤。第４ 周起，两感染组大鼠各级支气管慢性炎症明显，管壁增厚（Ｐ＜０－０１） ，管腔明显狭窄（Ｐ＜０－０５）， 有肺气肿形成。两感染组ＲＶＳＰ明显升高（Ｐ＜ ０－０１）。细支气管伴行肺小动脉管壁明显增厚。第１６ 周， 肺炎克雷伯杆菌感染组ＰａＯ２ 下降（Ｐ＜０－０５） ，ＰａＣＯ２ 上升（Ｐ＜０－０１） 。结论　以适量肺炎克雷伯杆菌或肺炎链球菌多次经鼻腔注入大鼠肺内可引起小气道炎症和肺气肿。结合血气分析和ＲＶＳＰ变化情况证实，所建模型具有ＣＯＰＤ的主要特征。更多还原

【Abstract】 Objective To observe the role of bacterialinfection in pathogenesis of COPD- Methods The COPDanimal model was developed by intranasal repeated injecting Klebsiella pneumoniae(K) or pneumococcal pneumoniae(P) into rat respiratory tract- Histomorphyological changes were observed, PaO2, PaCO2 and right ventricularsystolicpressure(RVSP) wereanalysed- Results 1 weekafterinjecting Kand4 weekafterinjectingP,the epitheliaof bronchioles showed obviousinjury- From the 4th week there was severe chronic inflammatory process of bronchiolesin2 experimentalgroupsincludingthickened wall,narrowedlumenand developedemphysema-Inaddition, the wallsofarteriolesaccompanying bronchioles werealsothickened obviously- Rightventricularsystolic pressureraised in2 experimentalgroups(P<0-01)- Fromthe16th week,PaO2 droppedand PaCO2raisedin Kgroup- Conclusions Repeatedinjectingintranasallyofthe properamountofklebsiella pneumoniae orpneumococcalpneumoniaeintorats′ lungscaninduceratsmallairwayinflammation and emphysema- Combining with PaO2,PaCO2 and RVSPanalysis,we suggestthe modelestablished shows mainfeaturesofCOPD-更多还原