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 。
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.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2000年第12期713-715,共3页
Chinese Journal of Trauma
关键词
脑损伤
神经元内游离氢
液压撞击伤
Brain injuries
Hypothermia
Nimodipine
D-2-amino-5- phosphonovaleric acid
