利多卡因和硫喷妥钠对培养的大鼠海马脑片神经元损伤的影响

目的 :观察利多卡因和硫喷妥钠对生后 2 2d大鼠培养海马脑片的实验型缺血后神经元损伤的影响。方法 :将培养的SD大鼠海马脑片实验型缺血 (缺氧缺糖 ) 1 0min ,给药组在缺血前 1 0min给予 1 0nmol/L、1 0 0nmol/L的利多卡因或 2 50nmol/L、60 0nmol/L的硫喷妥钠 ,缺血后换用正常培养基继续培养 7d ,并用荧光染料PropidiumIo dide(PI)连续观察海马CA1区和齿状回神经元的损伤。结果 :缺血后第 1d缺血组即出现神经元损伤高峰 ,CA1区和齿状回的PI指数显著增加 (P <0 .0 1 ) ;直至缺血后第 7d其损伤指数仍显著高于缺血前水平 (P <0 .0 1 )。两浓度的利多卡因和硫喷妥钠均可降低缺血后CA1区和齿状回神经元损伤的程度 (P <0 .0 1 ) ,并可将CA1区和齿状回的神经元损伤高峰推迟至缺血后第 3d。结论 :利多卡因和硫喷妥可减轻缺血后海马CA1区和齿状回的神经元损伤 ,推迟神经元的损伤高峰。

Effects of lidocaine and thiopental on the neuronal injury in rat hippocampus slice cultures

Aim: To observe the effects of lidocaine and thiopental on the neuronal injury induced by the experimental ischemia in hippocampus slice cultures obtained from postnatal 22 days SD rats. Methods: Model of the experimental ischemia was produced by hypoxia and glucose deprivation. Propidium iodide(PI) assay was used to observe the neuronal injury in CA1 and dentate gyrus(DG). Results: After experimental ischemia, the peak of PI index was appeared in CA1 and DG on the first day( P <0.01), PI index in DG was less than in CA1( P <0.01). PI indeces were still higher during seven days after the experimental ischemia than before the experimental ischemia( P <0.01). 10 nmol/L and 100 nmol/L concentration of lidocaine could significantly decrease PI indeces in CA1 and DG( P <0.01). 250 nmol/L and 600 nmol/L concentration of thiopental also decreased the PI indeces in CA1 and DG( P < 0.01 ). The neuronal injury peaks were postponed to the third day after the experimental ischemia by lidocaine and thiopental. Conclusion: It suggested that lidocaine and thiopental could decrease the neuroal injury in CA1 and DG induced by the experimental ischemia, and postpone the neuronal injury peaks to the third day after the experimental ischemia.