【摘要】 本研究旨在应用经典玻璃微电极方法观察植物性雌激素三羟异黄酮 (genistein ,GST)对家兔房室结细胞自发活动的电生理效应及其作用机制。GST (10～ 10 0 μmol/L)不仅以剂量依赖性方式抑制房室结起搏细胞的动作电位 0相最大上升速度 (Vmax)、4期去极化速率 (VDD)、自发起搏频率 (RPF)和动作电位幅值 (APA) ,而且延长复极化90 %的时间 (APD90 )。如提高灌流液中钙离子浓度以及应用L型钙通道开放剂BayK864 4(0 2 5 μmol/L) ,则可拮抗GST对起搏细胞的上述电生理效应 ,但NO合酶阻断剂L NAME (0 5mmol/L)对GST的效应并无影响。以上结果提示 ,GST可抑制家兔房室结的自发活动 ,这些效应可能与其抑制钙离子内流有关 ,但此作用机制中并无NO参与。更多还原

【Abstract】 The purpose of this study was to determine the electrophysiological effects of genistein (GST) on spontaneous activity of atrioventricular (AV) node and the underlying mechanism(s). Action potentials in AV node cells were recorded using intracellular microelectrode technique. GST not only reduced the amplitude of action potential (APA), maximal rate of depolarization (V max ), velocity of diastolic (phase 4) depolarization (VDD), and rate of spontaneous firing (RSF), but also prolonged 90% duration of action potential (APD 90 ) in a concentration dependent manner. The effects of GST (50 μmol/L) could be blocked completely by pretreatment with Bay K8644 (0 25 μmol/L), an agonist of L type calcium channel. Pretreatment with N G nitro L arginine methyl ester ( L NAME, 0 5 mmol/L), a nitric oxide (NO) synthase inhibitor, did not affect the effects of GST on AV node cells. Elevation of Ca 2+ concentration (5 mmol/L) in superfusate antagonized the effects of GST (50 μmol/L). These results suggest that GST exerted a negative electrophysiological effects of spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but had no association with NO release.更多还原