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目的研究双苯氟嗪(D ip)对异丙肾上腺素诱发人心房肌纤维迟后除极(DAD s)和触发活动(TA)的影响。方法应用异丙肾上腺素诱发稳定且可重复的迟后除极和触发活动。用细胞内玻璃微电极技术记录DAD s和TA诸参数。结果预先应用D ip(3μmol.L-1)或乙醇溶剂(3 mL.L-1)对异丙肾上腺素引起的DAD s和TA无明显影响;D ip(10μmol.L-1)使DAD s的幅度从(13.3±2.3)mV降低到(4.0±1.0)mV,但对DAD s和TA的发生率无显著影响;D ip(30μmol.L-1)则能抑制DAD s和TA的发生。结论D ip对异丙肾上腺素诱发的人心房肌纤维DAD s和TA有抑制作用,这可能与其抑制L-型钙通道和/或肌浆网钙释放从而减轻细胞内钙超载有关,并可能由此产生抗心律失常作用。
Objective To investigate the effect of dipfluzine (Dip) on isofemoral-induced atrial fibrillation after delayed depolarization (DAD s) and triggering activity (TA). Methods Isoproterenol was used to induce stable and repeatable depolarization and triggering activities. DAD s and TA parameters were recorded using intracellular glass microelectrode technology. Results DAD and TA induced by isoproterenol were not affected by pretreatment with D ip (3μmol.L-1) or ethanol (3mL.L-1). DAD (10μmol.L-1) Decreased from (13.3 ± 2.3) mV to (4.0 ± 1.0) mV, but had no significant effect on the incidence of DAD s and TA. D ip (30 μmol·L -1) inhibited the incidence of DAD s and TA. Conclusions D ip inhibits isoprenaline-induced DAD s and TA in human atrial myofibers, which may be related to its inhibition of calcium release from L-type calcium channel and / or sarcoplasmic reticulum and thereby the decrease of intracellular calcium overload, Anti-arrhythmic effect.