兔海水淹溺肺水肿发生机制的实验研究  

Study on the Mechanism of Pulmonary Edema after Seawater Drowning in Rabbit

作　　者：董文度[1] 刘新卷[1] 傅更锋[1] 丁勇 张敏华[1] 骆云[1] 王琰[1] 刘虹[1] 徐根兴[1] 赵增荣[1] 袁驾南 

机构地区：[1]第二军医大学南京军医学院分子医学研究所,南京210099

出　　处：《生物医学工程学杂志》2000年第2期196-201,205,共7页Journal of Biomedical Engineering

基　　金：中国人民解放军总后医药卫生立项课题!96M036

摘　　要：为探讨海水淹溺肺水肿（PE－SWD）的发生机理，应用丹麦产ABL-Ⅲ型血气-酸碱分析仪，对兔动脉血气和酸碱指标进行自动检测；采用计算机图像分析系统，对肺Na+－K+－ATPase、细胞色素氧化酶（CYTO）和碱性磷酸酶（ALP）进行自动检测和定量分析；采用原位杂交和免疫组化技术，对肺组织C－fosmRNA和Fos蛋白进行定量检测；采用磷脂和Ca2+超微结构定位方法，对肺磷脂和Ca2+的分布进行定位定量观察。结果表明：PE-SWD组动脉氧分压（PaO2）、血氧饱和度（SaO2）、pH值、实际碳酸氢盐（AB）、剩余减（BE）、肺Na+－K+－ATPase和CYTO显著降低。PE－SWD组兔肺上皮组织中ALP、c－fosmRNA和Fos蛋白的表达水平比正常对照组（NC）明显升高（P＜0.01）。PE－SWD组肺泡Ⅱ型上皮细胞磷脂反应产物明显减少，肺毛细血管内皮细胞和肺泡Ⅰ、Ⅱ型上皮细胞Ca2+沉淀颗粒明显增多。作者认为，海水损伤性作用、低氧血症和代谢世酸中毒是PE－SWD发生机制中三种重要因素。肺Na+－K+－ATPase、CYTO活力降低和细胞内钙超载既是上述三大因素造成的直接恶果，又是促进PE－SED不断发生发展的继发性原因。Ca2+－fos传导途径可能也是导致PE－SWD不断恶化的重要环节。To study the mechanism of pulmonary edema after seawater drowning (PE-SWD), the indexes of blood-gas and acid-base in rabbits artery blood were measured by the blood-gas analyser. The activity of Na+-K+-ATPase, cytochrome oxidase (CYTO) and alkaline phosph arase(ALP) in the lungs were measured and analysed by computer image system. C-fos mRNA and Fos protein in the lungs were respectively determined by situ hybrioization and immunohisto chemical techniques. The distribution of phospholipid and Ca2+ of rabbits lungs was quantitatively analysed by ultrastructual location method. The results showed that, five parameters of PaO2,oxygen saturation(SaO2), pH, actual bicarbonite (AB) and base excess(BE) and the activity of Na+-K+-ATPase and CYTO decreased remarkably in PE-SWD. Both c-fos mRNA and Fos protein expression in pulmonary epithelial'cells in PE-SWD were significantly elevated compared with the normal controls (P＜0.01). The phospholipidsproducts in the pulmonary alveolar type Ⅱ epithelial cells were decreased, however, the Ca2+ precipitate pellets inside the lung capillary endothelial cells and the pulrnonary alveolar type Ⅰ and Ⅱ epithelial cells increased obviously. The arthors suggest that the injuny action of the seawater, hypoxia and metabolic acidosis may be the mianthree mechanisms of the pulmonary edema induced seawater drowning. The lowering activity of Na+-K+-ATPaseand CYTO in the lungs and calcium overload in the cells are not only evil consequence resulted from above threefactors, but also the importent causes leading to the worse of PE-SWD. The transmiting line of Ca2+-fos may bealso a key link to bring about the worse of PE-SWD.

关 键 词：海水淹溺 肺水肿 细胞色素氧化酶 C-FOS基因 

分 类 号：R363[医药卫生—病理学]