液压撞击伤后神经元内游离氢的变化及其影响因素

目的 研究液压撞击伤时体外培养的单个大鼠神经元内游离氢（〔Ｈ＾＋〕ｉ）的变化，探讨尼莫地平（Ｎｉｍ、Ｄ－２－氨基戊酸（Ｄ－ＡＰ－５）和亚低温对创伤后神经元内〔Ｈ＾＋〕ｉ变化的影响及机制。方法 以ＢＣＥＣＦ／ＡＭ为细胞内氢离子的荧光指示剂，用激光共聚焦显微镜测定液压撞击伤时体外培养的大鼠神经元内〔Ｈ＾＋〕ｉ的变化。结果 液压撞击伤后脑皮质神经元〔Ｈ＾＋〕ｉ于伤后１５ｍｉｎ即已升高（Ｐ〈０．０１），１

Changes of [H+]i in neurons following hydraulic impact injuries and effective factors in rats

Objective To investigate alteration in [H ]i of Wistar rat's neuronal cell following hydraulic impact injury and the effect of nimodipine(Nim),D 2 amino 5 phosphonovaleric acid(D AP 5) and mild hypothermia on change of neuronal [H ]i following trauma. Methods Alteration in [H ]i in Wistar rat's neuronal cell following hydraulic impact injury was measured by means of a confocal laser scanning microscope using BCECF/AM as a hydrogen indicator. Results [H ]i in neuronal cell subjected to hydraulic impact injury increased at 15 min post-injury ( P <0.01), went up to the peak value at 12 h post-injury, afterwards decreased gradually and still maintained a higher level at 48 h post-injury ( P <0.001).Optimal application of Nim following hydraulic impact injury was within 4 h post-injury ( P <0.01), optimal application of D AP 5 following hydraulic impact injury was within 10 h post-injury, mild hypothermia was used to inhibit [H ]i within 30 min post-injury. Application of D AP 5 within 4 h post-injury was superior to Nim ( P <0.001). Conclusions Intracellular acidosis occurs following hydraulic impact injury. Nim,D AP 5 and mild hypothermia can decrease [H ]i, but the time windows following hydraulic impact injury are different, suggesting that to treat neuronal acidosis following traumatic brain injury (TBI) should combine multiple treatments with their optimal time windows.