呼吸道合胞病毒细支气管炎、肺炎的发病机理研究  

STUDIES ON THE PATHOGENESIS OF RESPIRATORY SYNCYTICALVIRUS BRONCHIOLITIS AND PNEUMONIA

作　　者：张家驹[1] 刘菊华[1] 杜景云[1] 张忠玲[1] 陈卫宁[1] 

机构地区：[1]山东省医学科学院

出　　处：《山东医科大学学报》1999年第2期106-108,共3页Acta Academiae Medicinae Shandong

基　　金：山东省科委科研基金

摘　　要：为探讨ＲＳＶ感染导致的细支气管炎和肺炎的发病机理，以ＲＳＶ感染棉鼠和小白鼠为动物模型，利用光镜、透射电镜和扫描电镜观察鼠肺组织的病理变化，并分离病毒。感染第５天时，肺微血管内充以大量嗜酸性粒细胞、淋巴细胞、单核细胞。柱状纤毛上皮细胞、基底细胞和Ｃｌａｒａ细胞脱落、坏死。嗜酸性粒细胞和肥大细胞多呈活化和脱颗粒状态，释放于固有层和上皮细胞之间。感染第８天后，上述变化明显减轻，但未完全恢复。提示ＲＳＶ致过敏反应是重要病因，肺泡腔内嗜酸性粒细胞聚集是该病的重要病理特征。Respiratory syncytical virus(RSV) is the main cause of pulmonary infection of the infant and elder. In order to explore the pathogenesis, The authors used RSV infected cotton rats and mice as animal models. With the optical microscope, transmission electron microscope(TEM), scanning electron microscope(SEM) and virus isolation techniques, a lot of lymphocytes, monolytes, neutrophil leukocytes and acidophilicleukocytes were full in microvessels of bronchiole and alveolar of lung after the 5th day of RSV infection. Lymphocytes congregated near smallvessels. By TEM and SEM, the columnar ciliary epithelium cells, basal cells and clara exfoliative cells and necrosis were also discovered. Acidophilic leukocytes and mastocytes show active degranular state, and were released between lamina propria and epithelium cells. On the 8th day of infection, the inflammation was reduced, but without completely recovery. The results show that allergic reaction after RSV infection played an important role in the criti

关 键 词：呼吸道合胸病毒 肺炎 细支气管炎 病理学 

分 类 号：R562.210.2[医药卫生—呼吸系统] R563.102[医药卫生—内科学]