【摘要】 目的研究同型半胱氨酸对豚鼠心房肌细胞钠通道的作用。方法应用Langendorff装置分离单个豚鼠心房肌细胞,运用全细胞膜片钳技术检测同型半胱氨酸对心肌离子通道的作用。结果同型半胱氨酸可以明显地增加豚鼠心房肌细胞上的钠电流,50μmol/L同型半胱氨酸可以增加钠电流47.1%,而500μmol/L同型半胱氨酸可增加钠电流115.7%,同型半胱氨酸对钠电流作用的半数有效浓度为(90.8±18.6)μmol/L,50μmol/L同型半胱氨酸可使钠通道的最大激活电位由-30mV升至-20mV;而通道动力学研究显示,同型半胱氨酸可以明显地延迟钠通道的失活和加快钠通道的复活。结论同型半胱氨酸可以明显地增加豚鼠心房肌细胞钠电流,改变钠通道的最大激活电位,其主要是通过抑制钠通道失活过程增加钠电流的幅度。更多还原

【Abstract】 Objective To investigate the effects of homocysteine on sodium currents in guinea pig atrial myocytes and explore potential mechanisms by which homocysteine was related to atrial fibrillation.Methods Enzyme digestion method was used to isolate single guinea pig atrial myocytes and whole-cell patch clamp technique was used to record sodium currents.Results In atrial myocytes of guinea pig,50μmol/L,500μmol/L of homocysteine increased sodium currents by 47.1% and 115.7%,respectively.The medium effective concentration for increase of sodium currents by homocysteine was (90.8±18.6)μmol/L,and 50μmol/L homocysteine significantly changed maximal activation test potential from-30mV to-20mV.Gating kinetic data of sodium channel showed that homocysteine shifted inactivation and recovery curve to negative potentials but did not obviously affect the activation curve.Conclusion Homocysteine can increase sodium currents by slowing the inactivation of sodium currents in isolated atrial myocytes in guinea pig.更多还原