小鼠急性双光气中毒后肺水肿的超微结构基础  

Ultrastructural basis of pulmonary edema in mice after exposure to diphosgene

作　　者：杜忠民[1] 臧建申 王冰枫[2] 

机构地区：[1]第四军医大学放射医学教研室 [2]第四军医大学病理学教研室

出　　处：《第四军医大学学报》1992年第3期213-216,共4页Journal of the Fourth Military Medical University

摘　　要：作者用雄性昆白小鼠20只分两批于动力中毒柜中吸入双光气中毒,浓度分别为125μg/L和122.5μg/L,中毒时间10 min.中毒后1,2,4,8,12 h分批处死,处死前15 min静脉内注入辣根过氧化物酶,以研究肺水肿的发生过程及液体的运行途径.电镜观察显示细支气管上皮细胞、肺泡上皮细胞、血管内皮细胞等有明显的损伤性变化,示踪物一般不通过肺泡上皮细胞的紧密连接,但损伤严重处可见水肿液、纤维素及示踪物直接溢入肺泡腔,说明气血屏障,尤其是薄部损伤是肺水肿液体渗出的超微结构基础.Twenty mice in 2 batches were exposed to diphosgene at the concentration of 125 μg/L and 122.5μg/L for 10 minutes. The mice were injected intravenously with horseradish peroxidase (HRP) as a tracer 15 minutes before sacrifice. Localization of HRP was performed 1. 2, 4, 8, 12 h after exposure, in order to examine the permeability of the alveolar wall and the pathway of fluid leakage in pulmonary edema. It was found that the ultra-structural injury of the epithelial cells of bronchiolar, endothelial cells of capillary and alveolar epithelial cells were prominent. The tight junctions of pneumocytes normally prevented the passage of fluid and HRP tracer, but in the severe damage area, direct leakage of edematous fluid and HRP tracer into the alveolar spaces could be found through the endothelium, basement membranes, interstitial tissue and pneumocytes. These foundings suggest that the injury of the thin part of air-blood barrier is the basis of fluid leakage in pulmonary edema after diphosgene poisoning.

关 键 词：光气 中毒 肺水肿 超微结构 

分 类 号：R818.03[医药卫生—放射医学]