二次脑损伤神经细胞内游离Ca^(2+)、脑组织丙二醛与血液流变性的改变

Changes in neuronal Ca^(2+),malondialdehyde in brain tissue and hemorrheology after secondary brain insults

目的 :探讨脑弥漫性轴索损伤 (DAI)及合并二次脑损伤 (SBI)的发生机制。方法 :12 0只大鼠随机分为正常对照、单纯 DAI及合并 SBI(低血压与高热 )组 ,于伤后 0 .5、3、12、2 4和 72小时检测神经细胞内游离 Ca2 + 、自由基和血液流变学指标。结果 :DAI后神经细胞内游离 Ca2 + 超载明显 ,0 .5小时即有表达 ,12小时达高峰 ,持续至 2 4小时 ;在伤后同一时间点 ,与单纯 DAI组比较 ,DAI合并 SBI组 Ca2 + 含量明显增加 (P<0 .0 5 )。 DAI后自由基与血液粘滞性指标在伤后 3小时开始增高 ,2 4小时达高峰 ,72小时开始下降 ;与单纯 DAI组比较 ,DAI合并 SBI组丙二醛 (MDA)和血液粘滞性指标均明显高于相应时间点单纯 DAI组 ;脑组织中 MDA含量与全血粘度、血细胞比容、红细胞聚集指数呈正相关 ,组织病理学改变 SBI较单纯 DAI重。结论 :神经细胞 Ca2 +超载是DAI及 SBI发生机制的关键 ,自由基和血液流变学特性改变也起重要作用。

Objective:To study the significance of changes in neuronal Ca 2+ ,malondialdehydes(MDA) in brain tissue and hemorrheology in a rodent model of diffuse axonal injury (DAI) with secondary brain insults (SBI).Methods:One hundred and twenty male rats were randomized into control,DAI alone and DAI with SBI (hypotention and hyperthermia) groups.The neuronal Ca 2+ ,MDA in brain tissue and hemorrheology were observed at 30 minutes,3,12,24 and 72 hours following injury.Results:The neuronal Ca 2+ overload began at 30 minutes,peaked at 12 hours and continued till 24 hours after DAI.The neuronal Ca 2+ overload increased remarkably(P<0 05) in DAI with SBI group compared with that of DAI alone at the same time point.Meanwhile,there were positive correlations between MDA and whole blood viscosity,hematocrit and red blood cell aggregation index.The above mentioned parameters began to increase at 3 hours after injury,peaked at 24 hours and decreased at 72 hours.MDA and blood viscosities in DAI with SBI group were also significantly higher than those in DAI alone group at the respective time intervals.Pathological examination showed more severe injury in DAI with SBI compared with DAI alone.Conclusions:The neuronal Ca 2+ overload play a pivotal role in the development of DAI and SBI,and changes of free radicals and hemorrheology after brain injury might also contribute to SBI leading to brain damage.