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作 者:柳国胜[1] 赵立华[1] 聂川[1] 罗先琼[1] 邱锐琴[1] 康举龄[2] 唐福星[3] 郭祖文[3]
机构地区:[1]暨南大学附属第一医院儿科,广东广州510630 [2]暨南大学附属第一医院病理科,广东广州510630 [3]暨南大学附属第一医院电镜室,广东广州510630
出 处:《暨南大学学报(自然科学与医学版)》2005年第6期781-786,共6页Journal of Jinan University(Natural Science & Medicine Edition)
基 金:广东省卫生厅科研基金(2003379);国家教委教外司基金[1999]363资助项目
摘 要:目的:探讨新生大鼠在高氧肺损伤不同时点肺组织各种细胞超微结构的改变。方法:99只新生大鼠随机分为高氧组和空气组,生后3、7和14 d分批处死并取肺组织进行H.E染色病理检测,电镜检查各组肺组织的超微结构改变。结果:1)高氧组肺损伤主要表现为肺泡结构破坏、大小不一、肺间隔增厚以及胶原纤维沉积。2)超微结构主要表现为肺泡Ⅱ型细胞板层小体空泡化、肺泡Ⅰ型细胞胞浆溶解,成纤维细胞胞浆中的内质网、高尔基体和线粒体增多,肺泡Ⅰ型和Ⅱ型细胞线粒体肿胀等改变。结论:肺泡Ⅱ型细胞的不成熟、肺泡Ⅰ型细胞的变性和成纤维细胞合成胶原能力增强是导致高氧肺损伤病理改变的基础。Aim: To explore the change of ultrastmcture in the lung of neonatal rats exposed to hyperoxia at different time. Methods: Ninety - nine neonatal rats were assigned to hyperoxic group and air group nmdomly, they were sacrificed at the postnatal 3nt , 7th and 14th day respectively, then their lungs were harvested for H. E staining, and the changes of ultrastmcture were observed with electron microscope. Results: (1) Hyperoxic lung injury was mainly featured with destroyed alveoli, thickened alveoli septum and the deposition of collagen fibers. (2) Empty multlamellar bodies, cytoplasmolysis were found in type Ⅱ and Ⅰ alveolar cells respectively, mitochondrial swelling was observed in type Ⅱ、Ⅰ alveolar cells and endothelial cells, and organells such as endoplasmic reticulum,Golgi apparatus and mitochondrions increased in the cytoplasm of fibroblasts were presented. Conclusion: Undeveloped type Ⅱ alveolar cells, degenerative type Ⅰalveolar cells and intensive ability of collagen synthesis by fibroblasts are the pathological basis that lead to lung injury exposed to hyperoxia.
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