摘要
目的 :进一步探讨重型颅脑外伤后继发性呼吸衰竭的发生机制 ,为临床救治提供实验依据。方法 :利用打击伤大鼠模型 ,用电镜组织化学方法观察额顶叶打击伤后大鼠延髓超微结构及细胞内 Ca2 + 积聚的改变 ,及尼莫通 (Nim)、地塞米松的干预作用。结果 :打击伤使延髓细胞内 Ca2 + 积聚增加 ,Ca2 + 积聚以胞浆、线粒体及髓鞘为主 ,细胞超微结构破坏 ;重伤组较轻伤组变化明显 ;Nim可明显减少伤后细胞内 Ca2 + 积聚 ,并能改善细胞器的损伤。结论 :重型颅脑外伤导致延髓细胞 Ca2 + 超载可能是继发性呼吸衰竭的发生原因之一 ,Nim通过减少细胞内 Ca2
Objective:To investigate the mechanism underlying secondary respiratory failure following severe brain trauma,and to provide experimental evidence for clinical treatment.Methods:Using a rat model of blunt brain trauma,the changes in medullary ultrastructure and accumulation of intracellular calcium (Ca 2+ ) were observed by electromicroscope and histochemistry,and the effects of Nimotop (Nim) and dexamethasone (Dex) on blunt cerebral trauma were observed too.Results:After blunt cerebral trauma,increased accumulation of Ca 2+ in medullary cells and defective ultrastructure were found,and they were correlated with the degree of impact force.Treatment with Nim and Dex could reduce the accumulation of Ca 2+ ,and Nim had benefical effect in attenuating the ultrastructure damage.Conclusions:Ca 2+ overload in medullary cells induced by severe brain trauma may be one of important factors contributing to secondary respiratory failure,and Nim has beneficial effect by reducing accumulation of Ca 2+ in medullary cells.
出处
《中国危重病急救医学》
CAS
CSCD
2000年第12期714-716,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目(No.39800039)
