【摘要】 应用膜片箝技术记录游离豚鼠心肌细胞钠通道电流 ,细胞内微电极技术记录心室乳头肌的动作电位和心电图机记录豚鼠的心电图。使用与心肌细胞钠通道有高度亲和力的海葵毒素 (seaanemonetoxin ,ATXⅡ )改变钠通道开放的动力过程 ,从三个水平来研究钠通道、动作电位、心电图变化的关系 ,并试图探讨长QT综合征 (longQTsyndrome ,LQTs)的发病机制。结果显示 :ATXⅡ使钠通道的开放频率增加 ,钠通道中“长时间开放模式”的开放时间常数增大 ,动作电位的持续时间APD50 和APD90 也分别增加了 2 3%和 2 7%。ATXⅡ使动物心电图QT间期延长18 6 % ,QTc (校正的QT间期 )增大 18 9%。这些结果提示 ,钠通道动力过程的变化对动作电位和心电图QT间期有重要影响 ,钠通道功能或结构的变异可能是临床上部分长QT综合征产生的原因更多还原

【Abstract】 Single sodium channel currents were recorded by patch clamp technique in isolated guinea pig ventricular myocytes, and action potentials of papillary muscle and ECG were conventionally measured. Sea anemone toxin (ATXⅡ), a high affinity toxin to sodium channel, was used to change the sodium channel dynamics. Changes in the duration of action potentials and the QT interval of ECG depending on the channel modes were studied in order to provide hints to an understanding of pathogenesis of the long QT syndrome (a genetic disease). With the binding of ATXⅡ to the sodium channel, the occurrence frequency and the open time constant of the “long opening” mode of single Na channels increased significantly, whereas the action potential durations, APD 50 and APD 90 , were prolonged by 23% and 27% respectively. Following application of ATXⅡ, on the other hand, the QT interval and the QTc, a rectified QT interval, increased by 18. 6% and 18. 9% respectively. The results suggest that the dynamics or modes of Na channel play an important role in determining the action potential duration and the QT interval of ECG. The dynamical changes in Na channels induced by genetic mutation may be partially responsible for the long QT syndrome. [WT5HZ]更多还原