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目的:探讨内毒素与博莱霉素所致肺损伤的病理特征及肺泡Ⅱ型上皮细胞形态和功能的变化。方法:将60只SD大鼠随机分为内毒素组、博莱霉素组、对照组,内毒素组经尾静脉注射内毒素5 mg/kg,博莱霉素组给予气管内注入博莱霉素5 mg/kg,对照组气管内及尾静脉注入等体积的生理盐水。分别于给药后的第3,7,14,28天处死5只。肺组织HE染色及Masson染色行病理组织学检查及电镜观察其超微结构的改变。结果:内毒素组早期肺泡炎较重,短期内恢复正常,肺泡Ⅱ型上皮细胞主要表现为线粒体的水肿,板层小体的脱颗粒,增生不明显。博莱霉素组早期肺泡炎,随之出现纤维化,并逐渐加重。Ⅱ型上皮细胞变性坏死,线粒体破坏。结论:内毒素与博莱霉素虽均可导致肺损伤,前者恢复正常,后者演变成肺纤维化,可能与肺泡Ⅱ型上皮细胞损伤的程度有关。
Objective: To investigate the pathological features of lung injury caused by endotoxin and bleomycin and the changes of morphology and function of alveolar type Ⅱ epithelial cells. Methods: 60 Sprague-Dawley rats were randomly divided into endotoxin group, bleomycin group, control group and endotoxin group. Endotoxin was given 5 mg / kg through the tail vein and bleomycin group was given intratracheal injection of bleomycin Su-5mg / kg, control group of tracheal and tail vein injection of equal volume of saline. Five rats were sacrificed on days 3, 7, 14 and 28 after administration respectively. HE staining and Masson staining of lung tissue were performed histopathological examination and electron microscopy to observe ultrastructural changes. Results: In the endotoxin group, the early alveolitis was heavier and returned to normal in a short term. The type Ⅱ alveolar epithelial cells showed mainly mitochondria edema and lamellar body degranulation, with no obvious hyperplasia. Bleomycin group early alveolitis, followed by fibrosis, and gradually increased. Type Ⅱ epithelial cell degeneration and necrosis, mitochondrial damage. CONCLUSION: Although both endotoxin and bleomycin can cause lung injury, the former returned to normal, the latter evolved into pulmonary fibrosis, which may be related to the degree of alveolar type Ⅱ epithelial cell injury.