河豚毒素与硝苯吡啶对奎尼丁诱发的小鼠心房肌纤维早后去极化的影响(英文)

Effects of tetrodontoxin and nifedipine on quinidine-induced early afterdepolarization in atrial fibers of mice

在小鼠心房肌标本上研究了由奎尼丁诱发的早后去极化(EAD)。经奎尼丁(6.7μmol/L)处理并在长周期的驱动刺激下,EAD可稳定地发生,并显示其周长依赖性质。触发发放时程或数目与周长呈线性关系(两参数回归的γ值均为0.998,n=11)。奎尼丁诱发的EAD可由TTX(1.0μmol/L)或硝基吡啶(0.5-1.0μmol/L)所取消,并使动作电位时程恢复到正常值。结果提示I_(Na)(窗流)及I_(Ca)在EAD的发生上均有重要意义。

Early afterdepolarization (EAD) induced by quinidine was studied in mouse atrial preparations. EAD could be induced steadily by the treatment with quinidine (6.7 μmol / L) at a longer cycle length of the driving stimulation and showed its property of cycle length dependence. The relationship between the duration or number of triggered bursts and cycle length was linear (r value of the regression line was 0.998 in both parameters, n=ll). The quinidine-induced EAD could be abolished and the duration of action potential was recovered to normal value either by tetrodontoxin (1.0μmoL/L) or by nifedipine (0.5-1.0 μmol / L). It is suggested that both INa (window current) and ICa are significant in the genesis of EAD.