【摘要】 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 .0 1) ,12h达高峰 ,随后逐渐下降 ,48h仍维持较高水平 (P <0 .0 0 1)。Nim于伤后 4h内应用可降低 [H+ ]i,而D -AP - 5于伤后 10h之内应用有效 ,亚低温于 30min内应用可降低细胞内 [H+ ]i(P <0 .0 1)。其中在伤后 4h内D -AP - 5降低神经元细胞内 [H+ ]i的效果优于Nim(P <0 .0 0 1)。　结论　液压撞击伤致神经元内酸中毒 ,Nim、D -AP - 5和亚低温均降低细胞内[H+ ]i,但各自作用的有效时间窗不同 ,揭示对创伤后神经元酸中毒应注意综合治疗 ,并选定各自作用的最佳时间窗更多还原

【Abstract】 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.更多还原