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目的本实验用全细胞膜片钳技术研究氯胺酮与利多卡因对缺氧的培养大鼠海马神经元细胞Na+/K+电流的影响,从电生理角度为二者合用于临床而产生神经保护作用提供依据。方法取培养12d的海马神经元,随机分为正常对照N组,缺氧4hA组,加氯胺酮后缺氧4hK组,加利多卡因后缺氧4hL组,加氯胺酮及利多卡因后缺氧4hKL组,(两药均为100μmol/L,n=7)。全细胞记录法测量Na+/K+电流。结果①急性缺氧使培养海马神经细胞INa、IK电流降低(钳制电压-40mV至+60mV,P<0.05)。②与A组比,K、L、KL组INa在钳制电压为-30mV至+30mV时增加,KL组更显著(P<0.01)。③与A组比,K、KL组IK在钳制电压为+10mV至+60mV时增加,KL组更显著(P<0.01),L组无差别。结论氯胺酮及利多卡因合用时比单独使用更能提高体外海马神经元的钠钾通道完整性。
ObjectiveTo study the effect of ketamine and lidocaine on Na + / K + currents of hippocampal neurons cultured in hypoxia using whole-cell patch clamp technique, and to provide basis for the neuroprotective effects of both ketamine and lidocaine in clinical hippocampal neurons from electrophysiological point of view . Methods Hippocampal neurons cultured for 12 days were randomly divided into four groups: normal control group (n = 4), hypoxia group (4hA), hypoxia group (4hK group), hypoxia 4hL group after lidocaine plus hypoxia Group (both drugs are 100μmol / L, n = 7). Whole cell recording method to measure Na + / K + current. Results ① Acute hypoxia decreased INa and IK currents in hippocampal neurons (clamping voltage -40 mV to +60 mV, P <0.05). ② Compared with group A, INa in K, L, KL group increased at clamping voltage of -30mV to + 30mV, KL group was more significant (P <0.01). ③ Compared with group A, IK in K and KL group increased at clamping voltage of +10 mV to +60 mV, KL group was more significant (P <0.01), and L group had no difference. Conclusions Ketamine and lidocaine enhance the sodium and potassium channel integrity of hippocampal neurons in vitro when used alone.