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目的 研究莫索尼定 (Mox)对窦房结起搏细胞是否具有电生理作用及其相关受体以探讨Mox治疗实验性心律不齐的机理。方法 利用细胞内微电极技术记录窦房结细胞AP。结果 Mox(0 .3～ 3mmol·L- 1)浓度依赖性地降低AP的舒张期除极速率 (VDD) ,减慢自发搏动速率 (RPF) ,延长AP复极达 5 0 %及 90 %的时程 (APD50 和APD90 )。 1和 3mmol·L- 1Mox还明显增大最大舒张电位 (MDP)的绝对值。预先灌流α2 受体拮抗剂育亨宾 (1.0 μmol·L- 1,2 0min)取消Mox降低VDD ,延长APD50 和APD90 的作用 ;拮抗较低浓度Mox降低RPF和增大MDP的作用。育亨宾处理标本后 ,Mox显著增加AP幅度和最大除极速率。结论 Mox延长兔窦房结起搏细胞动作电位APD50 和APD90 以及降低VDD的作用主要由α2 受体中介。Mox增大MDP绝对值和减慢RPF的作用则与α2 受体部分相关
Objective To study whether moxodine has an electrophysiological effect on pacemaker cells of sinoatrial node and its related receptors in order to investigate the mechanism of Mox on experimental arrhythmia. Methods Intracellular microelectrode technique was used to record AP of sinoatrial node cells. Results Mox (0.3 ~ 3mmol·L-1) decreased AP diastolic depolarization rate (VDD), slowed spontaneous pulsatile rate (RPF) and prolonged AP repolarization up to 50% and 90% Schedule (APD50 and APD90). 1 and 3mmol · L-1Mox also significantly increased the absolute value of the maximum diastolic potential (MDP). Pre-perfusion of α2 receptor antagonist yohimbe (1.0 μmol·L -1, 120 min) abolished Mox decreased VDD, prolonged APD50 and APD90; antagonize lower concentrations of Mox reduce RPF and increase the role of MDP. After yohimbin treated specimens, Mox significantly increased AP amplitude and maximum depolarization rate. Conclusions Mox prolongs the action potentials of APD50 and APD90 in pacemaker cells of sino-atrial node and decreases the effect of VDD mainly mediated by α2 receptors. Mox increases the absolute value of MDP and slows down the role of RPF α2 receptor partial correlation