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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。
OBJECTIVE: To investigate the ultrastructural changes of lung cells in neonatal rats at different time points after hyperoxia-induced lung injury. Methods: Ninety-nine neonatal rats were randomly divided into hyperoxia group and air group. The rats were sacrificed at 3, 7 and 14 days after birth and the lungs were harvested for H.E staining. The ultrastructural changes of lung tissue were examined by electron microscopy. Results: 1) The lung injury in hyperoxia group mainly showed the destruction of alveolar structure, the different sizes, the thickening of lung space and the deposition of collagen fibers. 2) The ultrastructure mainly showed vacuolization of alveolar type II cell platelet, cytoplasmic lysis of alveolar type I cells, increase of endoplasmic reticulum, Golgi apparatus and mitochondria in cytoplasm of fibroblasts, Type mitochondria swelling and other changes. CONCLUSION: Immature alveolar type II cells, degeneration of alveolar type I cells and enhanced collagen synthesis by fibroblasts are the underlying causes of pathological changes in hyperoxic lung injury.