小鼠内毒素休克某些血液变化和细胞超微结构损伤的发生  

Alterations in blood and damage of ultrastructure in endotoxic shock of miceuang

作　　者：黄生宁[1] 郭炯[1] 

机构地区：[1]新疆医学院病理生理教研室

出　　处：《中国病理生理杂志》1994年第5期454-458,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金

摘　　要：小鼠内毒素休克有血液的乳酸、ＮＰＮ、ＡＫＰ、ＬＤＨ水平升高和ｐＨ值降低并可用６５４－２或ＡＬ所预防，只是预防ＮＰＮ升高的效应须在早期的肾血管挛缩消失后才能显示出来，心、肝、肠和肺的ＭＤＡ含量升高并可被６５４－２预防，除肺外还可被ＡＬ预防，将高肺ＭＤＡ只能用６５４－２预防结合注射内毒素后１０ｍｉｎ有ＷＢＣ入肺扣押来看，损伤肺的自由基可能主要来自被激活的中性粒细胞；血中ＡＫＰ和ＬＤＨ升高分别反映溶酶体膜和细胞膜受损；肝和肺的细胞有超微结构损伤性变化和硝酸镧颗粒进入并均可用６５４－２或ＡＬ所预防。The levels of lactate,nitride,AKP and LDH in plasma of endotoxic shock mice were increased,while the blood pH decreased,these were all prevented by 654-2 or AL;but the preventive effect on hypernitremia brought out only at the end of early constriction of renal vessel.MDA of heart,liver,lung and intestine,exceptkidney,were increased,which were all prevented by 654-2 or AL excepting lung.In view of the fact that the increase of pulmonary MDA was only prevented by 654-2 but not by AL,we suggested that lung was impaired by the free radical arised from the entrapped neutrophil cell.The increase in activity of AKP and LDH in plasma means that the membranes of cell and lysosome had injured or broken. Under electromicoscopy,he slight hydropic degeneration of cell and the granule of nitrite lanthanum assing into inside of cells were seen,which was also prevented by administration of 654-2 orAL before the shock.

关 键 词：内毒素 休克 丙二醛 乳酸脱氢酶 游离基 

分 类 号：R364.14[医药卫生—病理学]