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机构地区:[1]首都医科大学附属北京同仁医院麻醉科,100730
出 处:《北京医学》2011年第4期329-331,共3页Beijing Medical Journal
摘 要: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。Objective To evaluate the effect of ketamine and lidocaine on IK and INa of the anoxic responses in primary cultured hippocampal neurons.Methods The 12-day-cultrued hippocampal cells were randomly divided into five groups(n=7):normal control(group N),anoxia for 4 hours(group A),combined lidocaine and anoxia for 4 hours(group L),combined ketamine and anoxia for 4 hours(group K),combined lidocaine and ketamine and anoxia for 4 hours(group KL).IK and INa of whole-cell recorded by patch-clamp were performed for every group.Results ①Anoxia decreased IK and INa in the cultured hippocampus neurons (P0.05).②IK and INa in group L and K were increased than those in group A(P0.05),and more evident in group KL (P0.01).Conclusions Ketamine and lidocaine may enhance the tolerance of anoxia in primary cultured hippocampus neurons by increasing cell potassium and sodium current.
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