小鼠创伤性休克时血中糖、乳酸和NPN变化的发生  

Alterations of plasma glucose,lactate and NPN in mouse traumatic shock

作　　者：江明[1] 郭炯[1] 

机构地区：[1]新疆医学院病理生理教研室,新疆医学院一附院血液科

出　　处：《中国病理生理杂志》1994年第4期398-402,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金

摘　　要：小鼠创伤性休克时血中糖、乳酸和ＮＰＮ升高。休克９０ｍｉｎ血糖开始回降，１２０ｍｉｎ骤降而成为死亡的先兆。６５４－２和ＡＬ可预防高乳酸血，对高氮质血无效，因为过多的含氮物主要来自破坏的组织而非代谢障碍。６５４－２可使高血糖曲线右移，延长存活时间，ＡＬ无此作用。除肾外，心、肝、肺均有ＭＤＡ升高；６５４－２可预防心、肝的ＭＤＡ升高而对肺无效；ＡＬ可预防肺、肝ＭＤＡ升高而对心无效；提示不同器官的自由基来源不同。诸器官中只有肝的ＬＤＨ活性升高并可被６５４－２和ＡＬ预防。血胰岛素降低并可被ＡＬ所预防；血皮质醇有应激性升高且不受６５４－２和ＡＬ的影响。电镜下有肝细胞受损并可被６５４－２和ＡＬ预防。In traumatic shock mouse,the plasma level of glucose,lactate and nitriderose rapidly.At 90 min after shock the hyperglycemia began to fall back,it fell sharply at120 min which was the crisis or prodrome of death,654-2 and AL (allopurinol)wouldprevent the reappearance of lactate, but they would not prevent the hypernitraemia because theexcessive extranitride in plasma was primarily came from ruptured tissue not from metabolicdisturbance.The hyperglycemic curve shifted to the right and the surviveal time was pro-longated in animal pretreated with 654-2, which was not seen in animals pre-treated withAL.MDA of heart,liver and lung except kidney, was increased,654-2 could prevent theincrease of MDA in heart and liver but not in lung;AL could prevent the increase ofMDA in lung and liver while not in heart.Thase results indicated that the source of freeradical in each organ was different.In the above organs,only the LDH cativity in liverincreased,which was prevented by 654-2 or AL.The plasma insulin level decreased whichcould be prevented by AL.Blood cortisol was increased by stress,was not influencedby 654-2 or AL.The damages of hepatocytes were seen under electromicroscopy,and wereprevented by 654-2 and AL.

关 键 词：休克 创伤性 血乳酸 自由基 

分 类 号：R441.9[医药卫生—诊断学]