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目的：为进一步观察ＩＨＣ－６６的电生理特性，探讨其抗心律失常的作用机制。方法：采用离体豚鼠窦房结、乳头状肌及部分除极化乳头状肌标本，观察了３，６－ｄｉ（ｄｉｍｅｔｈｙｌａｍｉｎｏ）－ｄｉｂｅｎｚｏｐｙｒｉｏｄｏｎｉｕｍｏｆｆｅｒｉｃＥＤＴＡ（ＩＨＣ－６６）对不同类型心肌细胞电活动的影响。结果：ＩＨＣ－６６１０μｍｏｌ·Ｌ－１使窦房结细胞动作电位４相除极速率（ＳＰ４）降低１１．４２％、增加动作电位复极９０％时程（ＡＰＤ９０）１８％、降低零相最大上升速率（Ｖｍａｘ）４７％、使部分除极化乳头状肌细胞动作电位（ＡＰ）之ＡＰＤ９０、动作电位复极５０％时程（ＡＰＤ５０）分别缩短９％、１３％，Ｖｍａｘ降低５８％，同时，ＩＨＣ－６６（１０、３０、５０μｍｏｌ·Ｌ－１）呈剂量依赖性降低Ｂａ２＋（２ｍｍｏｌ·Ｌ－１）诱发的自发性动作电位振幅（ＡＰＡ）与Ｖｍａｘ，缩短ＡＰＤ５０、ＡＰＤ９０，明显减慢自发性电活动的频率。结论：ＩＨＣ－６６的电生理学作用与其对慢内相电流的阻滞有关。
OBJECTIVE: To investigate the electrophysiological characteristics of IHC-66 and to explore its antiarrhythmic mechanism. Methods: The effects of 3, 6-di (dimethylamino) -dibenzopyriodonium of feric EDTA (IHC-66) on the electrical activity of different types of cardiomyocytes were observed using guinea pig sinoatrial node, papillary muscles and some depolarized papillary muscles. Results: IHC-6610μmol·L-1 decreased the 4-phase rate of action potentials (SP4) of sinoatrial node cells by 11.42% and increased APD90 by 18% and decreased the maximum increase of zero-phase (Vmax) of 47%, which reduced APD90, APD50 by 9%, 13% and Vmax by 58%, respectively. In a dose-dependent manner, IHC-66 (10,30,50 μmol·L-1) decreased the spontaneous action potential amplitude (APA) and Vmax induced by Ba2 + (2 mmol·L-1), shortened APD50 and APD90, Frequency of electrical activity. Conclusion: The electrophysiological effect of IHC-66 is related to the blockade of slow internal phase current.