瞬间冲击力致颅脑损伤过程中细胞内钙的变化

THE MECHANISM OF EXPERIMENTAL BRAIN INJURY FOLLOWING FLUID PERCUSSION IN RAT

目的 探讨瞬间冲击力致颅脑损伤过程中细胞内钙的变化及其作用机制。方法 使用可监控打击强度的流体冲击装置产生瞬间冲击力致大鼠中度脑损伤,伤后给钙通道阻断剂尼莫地平(0.04mg/kg,iv)。用荧光指示剂Fura-2/AM标记,检测脑损伤后脑海马细胞内游离钙的浓度,并作病理学观测。结果 脑损伤后细胞内游离钙明显增加,尼莫地平处理后,可明显地降低细胞内游离钙的浓度(P<0.01)和减轻细胞水肿。结论 瞬间冲击力介导颅脑损伤可能与神经细胞膜上钙通道开放、钙离子大量内流、引起钙超载有关。

Objective To observe the mechanism of traumatic brain injury (TBI) following fluid percussion in rats. Methods TBI was made by the fluid percussion device. The intracellular free calcium concentrations([Ca2+ ] i) of hippocampus in the TBI was detected by flouormeter with fluorchrome Fura - 2/ AM. Results [Ca2+ ]i was increased markedly with moderate TBI. Conclusion The calcium channel of cell membrane was open after TBI which could cause a large mount of calcium into cell inner, and increased concentration of intracellular free calcium. It might play an important role in the experimental brain injury.