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目的:研究糖尿病酮症酸中毒家兔I型肺泡上皮结构和功能的变化,探讨其损伤及修复机制。方法:新西兰家兔12只,随机分为实验组和对照组各6只,实验组给予链脲佐菌素(STZ)150 m.gkg-1和四氧嘧啶150 m.gkg-1,对照组给予等剂量生理盐水,72 h后检测动脉血气、尿酮体及血电解质,处死动物,取肺标本进行光镜、Ⅰ型肺泡上皮超微结构、Ⅰ型肺泡上皮酸性磷酸酶(ACPase)细胞组织化学等检查以及血小板衍生生长因子(PDGF)组织免疫化学检查。结果:实验组血气72 h后皆达到糖尿病酮症酸中毒标准;对照组正常。实验组光镜下可见肺泡腔内有明显渗出,肺泡腔见炎症细胞,肺泡隔增宽及肺出血;对照组无异常。PDGF免疫组织化学观察可见实验组肺泡壁和微血管内表达明显增高。实验组Ⅰ型肺泡上皮超微结构可见细胞膜结构模糊、基底膜增厚、细胞膜外高电子物质聚集等;对照组无异常。实验组动物细胞内ACPase活性也明显增强,溶酶体数量增多,形态不规则;对照组动物ACPase活性正常,全部存在于结构完整的溶酶体内。结论:糖尿病酮症酸中毒时Ⅰ型肺泡上皮细胞明显受损,细胞内ACPase活性增强,溶酶体数量增多,溶酶体的破坏对促进Ⅰ型肺泡上皮的损伤起了重要的作用;肺部在损伤的同时也启动了修复,PDGF参与了肺部修复的过程。
Objective: To study the changes of structure and function of type I alveolar epithelial cells in rabbits with diabetic ketoacidosis and to explore its mechanism of injury and repair. Methods: Twelve New Zealand rabbits were randomly divided into experimental group and control group with 6 rats in each group. The experimental group received 150 m.gkg-1 of streptozotocin (STZ) and 150 m.gkg-1 of alloxan, while the control group The rats were sacrificed and animals were sacrificed 72 hours later. The animals were sacrificed and lung specimens were taken for light microscopy, ultrastructure of alveolar epithelium type Ⅰ, histochemistry of type Ⅰ alveolar epithelial acid phosphatase (ACPase) Check and platelet-derived growth factor (PDGF) tissue immunohistochemistry. Results: The blood gas of the experimental group reached the standard of diabetic ketoacidosis after 72 h; the control group was normal. The experimental group showed obvious exudation of alveolar cavity under light microscope, inflammatory cells in alveolar cavity, alveolar septum broadening and pulmonary hemorrhage; the control group was normal. Immunohistochemical observation of PDGF showed that the expression of alveolar wall and microvessel in the experimental group was significantly increased. Experimental group Ⅰ alveolar epithelial ultrastructure showed fuzzy membrane structure, basement membrane thickening, high concentrations of extracellular plasma membrane accumulation; the control group without exception. The activity of ACPase in the experimental group was also significantly increased, the number of lysosomes increased, and the morphology was irregular. The ACPase activity in the control group was normal and all existed in the intact lysosome. CONCLUSION: Type I alveolar epithelial cells are obviously damaged in diabetic ketoacidosis, the activity of ACPase in cells is increased, the number of lysosomes is increased, and the destruction of lysosomes plays an important role in promoting the injury of type I alveolar epithelium. At the same time injury is also initiated repair, PDGF involved in the process of lung repair.