七氟烷增强单个培养鼠背根神经节细胞γ-氨基丁酸调控的氯电流

采用膜片钳全细胞记录和“Y型管”技术 ,观察七氟烷 (0 .38× 10 - 3 ～ 3× 10 - 3 m ol/L )对单个培养 SD鼠背根神经节细胞 3× 10 - 6mol/Lγ-氨基丁酸 (GABA )调控的氯电流影响 ,实验结果发现 ,0 .38× 10 - 3 ,0 .76× 10 - 3 ,1.5 2× 10 - 3 ,2 .2 8× 10 - 3 ,3.0 4× 10 - 3 mol/L七氟烷分别增强氯电流峰值高度至对照值的 (149± 2 5 ) % ,(2 0 3± 2 7) % ,(32 7± 79) % ,(331± 10 9) % ,(2 43± 71) %。实验结果提示 ,临床麻醉浓度的七氟烷能增强培养鼠背根神经节细胞 3× 10 - 6m ol/L

七氟醚抑制培养鼠迷走传入神经元5-羟色胺3受体调控的电流

目的与方法：采用膜片钳全细胞记录技术，观察０．７、１．４ｍＭ七氟醚对培养鼠结状神经节细胞３０μＭ二甲５－羟色胺引发的瞬间内向电流影响，并与氟烷、异氟醚作比较。结果：０．７、１．４ｍＭ七氟醚分别抑制５－羟色胺３受体调控的瞬间内向电流的峰值至对照值的７７％±１２％和６４％±９％。但氟烷、异氟醚均增强该电流。结论：结果提示临床麻醉浓度的七氟醚抑制鼠迷走传入神经元５－羟色胺３受体调控的瞬间内向电流。

七氟醚增强单个培养鼠背根神经节细胞γ-氨基丁酸调控的氯电流

目的 观察七氟醚 ( 0 38至 3× 10 -3 mol/L)对单个培养SD鼠背根神经节细胞 3× 10 -6mol/Lγ 氨基丁酸 (GABA)调控的氯电流影响。方法 采用膜片钳全细胞记录和“Y型管”技术。结果 0 38× 10 -3 ,0 76× 10 -3 ,1 5 2× 10 -3 ,2 2 8× 10 -3 ,3 0 4× 10 -3 mol/L七氟醚分别增强氯电流峰值高度至对照值的 149%± 2 5 % ,2 0 3%± 2 7% ,32 7%± 79% ,331%± 10 9% ,2 43%± 71%。结论 相关临床麻醉浓度的七氟醚能增强培养鼠背根神经节细胞 3× 10

联合使用异丙酚和地西泮对鼠感觉神经元γ-氨基丁酸调控的氯电流的影响

目的 研究联合使用异丙酚和地西泮对鼠感觉神经元γ氨基丁酸 (GABA)调控的氯电流的影响。方法 采用酶解和研磨技术游离SD幼鼠背根神经节细胞 ,选用膜片钳全细胞记录技术记录氯电流。 3μmol/LGABA采用压力喷射装置给予 ,溶解于细胞外液中的异丙酚 ,地西泮采用“Y型管”技术给药。结果 0 .3、1.0、3.0 μmol/L异丙酚和 10 0nmol/L地西泮联合作用于鼠感觉神经元所产生的由 3μmol/LGABA调控的氯电流峰值和曲线面积均明显大于二种药物单独使用所产生氯电流的理论之和 (P <0 .0 1)。地西泮使异丙酚增强GABA调控氯电流的浓度效应曲线左移 ,并降低异丙酚的EC5 0。结论 联合使用临床麻醉浓度的异丙酚和地西泮对鼠感觉神经元GABA调控的氯电流的增强效应产生协同作用。

异丙酚对单个培养鼠背根神经节细胞γ-氨基丁酸调控氯电流的影响

目的 观察异丙酚 (0 .1至 10× 10 - 6 mol/ L )对单个培养 Sprague- Dawley鼠背根神经节细胞 3× 10 - 6 mol/ Lγ-氨基丁酸调控的氯电流影响 ,从而探讨其麻醉机制。方法 采用膜片钳全细胞记录技术。结果 0 .1× 10 - 6 、0 .3× 10 - 6 、1× 10 - 6 、3× 10 - 6 、10× 10 - 6 m ol/ L异丙酚分别增强氯电流至对照值高度的 (10 8± 11) %、(131± 18) %、(191± 5 1) %、(2 72± 48) %、(798± 86 ) %。结论 临床麻醉浓度的异丙酚能增强 GABA调控的氯电流。

联合使用异丙酚和七氟醚对培养鼠背根神经节细胞γ-氨基丁酸调控的氯电流影响

目的 观察联合使用七氟醚和异丙酚对背根神经节细胞γ 氨基丁酸 (GABA)调控的氯电流影响。方法 采用酶解和研磨技术游离SD幼鼠背根神经节细胞 ,应用膜片钳全细胞记录技术记录氯电流 ,GABA采用压力喷射装置给予 ,溶解于细胞外液中的异丙酚、七氟醚则采用“Y”型管给药。结果 3× 10 -4 ,7× 10 -4 ,1 5× 10 -3 ,2 2× 10 -3 及 3× 10 -3 mol/L七氟醚分别增强氯电流至基础值的 149%± 2 5 % ,2 0 3%± 2 7% ,32 7%± 78% ,333%± 10 9%及 2 43%± 71%。 1× 10 -7,3× 10 -7,1×10 -6,3× 10 -6及 1× 10 -5mol/L异丙酚亦分别增强氯电流至基础值的 10 8%± 11% ,131%± 18% ,191%± 5 1% ,2 72 %± 48%及 789%± 86 %。二者联合使用后引发的氯电流高度与七氟醚、异丙酚分别产生的氯电流高度的理论之和的差异无显著性 (P >0 0 5 )。

Additive potentiation by co application of propofol and sevoflurane on GABA induced chloride current in cultured neurons from rat dorsal root ganglia

Objective To investigate the effects of various concentrations of sevoflurane and propofol and a combination of the two agents on chloride current induced by bath utilization of 3×10 -6 mol/L γ aminobutyric acid (GABA) in the rat dorsal root ganglia neurons maintained in primary culture Methods Sensory neurons from rat dorsal root ganglia were dissociated and cultured The whole cell patch clamp technique was used to record chloride current All drugs were applied with a rapid perfusion system, named “Y tube' method Results The peak chloride current amplitude was induced by 3×10 -6 mol/L GABA with substantially increasing of both sevoflurane and propofol Additionally, desensitization of I GABA induced by either propofol or sevoflurane was not observed We examined actions of various concentrations of propofol (3×10 -7 , 1×10 -6 , 3×10 -6 mol/L), sevoflurane (7×10 -4 mol/L) and their combination at concentrations relevant to clinical anesthesia on I GABA propofol(3×10 -7 , 1×10 -6 , 3×10 -6 mol/L) produced a concentration dependent increase in the response to 3×10 -6 mol/L GABA on I GABA When combined with 7×10 -4 mol/L sevoflurane, the potentiation of response to GABA obtained with various concentrations of propofol was not different from a theoretical additive response ( P >0 05) Conclusions Either sevoflurane or propofol and their combination at clinically relevant concentrations potentiate the GABA induced chloride current, which may at least partially contribute to the anesthetic mechanism Additive interaction obtained with a co application of propofol and sevoflurane may provide an evidence for a clinical combination of these two anesthetic agents

Propofol combined with diazepam synergistically potentiates the GABA-activated chloride current in rat sensory neurons

To investigate the effect of propofol combined with diazepam on the γ-aminobutyric acid (GABA)-activated chloride current (I GABA ) evoked in rat sensory neurons Methods Whole cell patch clamp recordings were made from cultured rat dorsal root ganglionic neurons GABA (3*!μmol/L) was applied by pressure ejection The anesthetics were dissolved in the external solution and given by the “Y-tube' method Results Co-application of propofol (0 3-3*!μmol/L) and diazepam (100*!nmol/L) potentiated the I GABA which was significantly larger than the sum of that potentiated by drug alone Diazepam (100*!nmol/L) shifted the concentration-response curve for the I GABA potentiation induced by propofol to the left in a parallel fashion The EC 50 value for propofol was decreased by diazepam from 7 6±1 8 *!μmol/L to 3 9±1 1*!μmol/L (n=9) Conclusions Our results suggest that propofol combined with diazepam synergistically potentiates the I GABA Diazepam-induced increase in the apparent binding affinity of propofol for the GABA A receptors is likely responsible for a clinical synergistic hypnotic action during co-application with propofol and diazepam