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作 者:孟凡寅[1] 陈玉林[1] 鲁彩霞[1] 许红[2] 张志鸿[2] 陈仕明[3] 王伟东[3]
机构地区:[1]上海第二军医大学烧伤研究所,200433 [2]复旦大学生理学和生物物理学系 [3]复旦大学生理学和生物物理学系测试中心
出 处:《中华整形烧伤外科杂志》1994年第6期447-451,共5页
基 金:国家自然科学基金
摘 要:我们采用25%TBSA Ⅲ度烧伤大鼠模型。考察了烧伤休克延迟复苏后红细胞膜蛋白结构、功能和运动等特性的改变。结果显示:烧伤休克延迟复苏后红细胞膜蛋白组份中出现高分子量交联蛋白(HMP),膜带3蛋白功能受损,膜蛋白侧向运动显著减弱,马来酰亚胺标记的大鼠红细胞膜在延迟复苏后其电子自旋共振波谱中强弱固定化作用谱的峰值比增大,旋转相关时间延长,膜蛋白的构象变化。实验证明:烧伤休克延迟复苏所造成的非典型的缺血——再灌注损伤通过膜蛋白表层巯基的氧化以及膜脂质过氧化作用引起了膜蛋白的交联,既改变了膜蛋白的构象,又削弱了膜蛋白的分子运动,进而可导致膜功能的异常。The dynamic properties of membrane protein are closely correlated to the membrane functions in erythrocytes.The anion transport function of band 3 protein,the constituents and the translational diffusion of membrane protein was detected in 25% TBSA burn rats.The changes in membrane protein SH were investigated by using the spin label of 3-maleimide-proxyl. The results showed that,in delayed fluid resuscitation group after burn shock, membrane crosslinking protein appeared in erythrocytes,the function of band 3 protein was damaged,the recovery time after fluorescence photobleaching of membrane protein was obviously prolonged,and the ratio of peak heights of strong to weak immobilization was increased,especially in the six-hour delayed resuscitation group,suggesting that the ischemia-reperfusion injury was more serious during the early shock stage.The authors believe that the results may represent the mechanism of damage biological membrane af- ter burns.The alterations of membrane properties caused by free radicals play an impor- tant role in erythrocyte injury.
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