脑损伤时脑突触体游离钙及脑皮质总钙量变化

The Changes of Concentration of Free Ca^(2+) within Brain Synaptosme and Total Contents in the Cortex Following Brain Injury

选用Wistar大鼠162只,采用细胞内荧光指标剂Fura—2检测脑损伤后不同时间脑皮质神经元突触体胞浆游离Ca^(2+)浓度([Ca^(2+)]i),并检测脑皮质总Ca^(2+)含量。结果表明,脑损伤后仅0.5小时,脑突触体游离[Ca^(2+)]i即已显著升高,为对照值的10倍;伤后6、24、48和72小时游离[Ca^(2+)]i持续处于超负荷状态,为对照值的16～17倍。脑损伤后脑组织总Ca^(2+)含量有一定程度增高,但难以反映神经细胞内Ca^(2+)超载的情况。实验结果提示,脑损伤后神经细胞Ca^(2+)超载是加剧脑继发性损害的重要因素之一。

The authors investigated the changes of free calsium [Ca^(2+)]i within brain synaptosme by using a new generation intracellular Ca^(2+) indicator——Fura—2/AM and the total Ca^(2+) content in cortex was determined in 162 male Wistar rats with brain injury. The results showed [Ca^(2+)]i within brain svnaptosme increased remarkablly and was ten times of that of the control a half hour after injury, and sixteen to seventee times at hour 6, 24, 48 and 72 after brain injury. The total Ca^(2+) content increased to some extend, but it was hard to indicate the Ca^(2+) overload within neurons. Our findings suggested that the neuronal Ca^(2+) overload might be the main cause of the subsequent brain lesion following primary brain injury.