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用常规玻璃微电极技术，观察３，６－（二甲氨基）－二苯骈碘杂环依地酸盐（ＩＨＣ－７２）对豚鼠右０００室乳头肌细胞膜部分除极引发的慢反应动作电位（ＳＡＰ）、哇巴因引发的延迟后除极（ＤＡＤ）及触发活动（ＴＡ）的影响。２．５４μＭＩＨＣ－７２对ＳＡＰ各参数均无影响；２５．４，１０１．６μＭＩＨＣ－７２分别使动作电位幅值（ＡＰＡ）减少７．４％和１９．３％，０相最大上升速率（Ｖ＿（ｍａｘ））减少２．５％和３９．１％，复极１００％的动作电位时程（ＡＰＤ＿（１００））缩短７．１％和４１％。有效不应期（ＥＲＰ）相对延长４．９％和９ｌ．３％，静息膜电位（ＲＭＰ）不受影响。浓度为２５．４μＭＩＨＣ－７２对复极５０％的动作电位时程（ＡＰＤ＿（５０））无影响，而浓度为１０１．６μＭ时能使ＡＰＤ＿（５０）缩短４２．９％，且能抑制由哇巴因诱发的ＤＡＤ及ＴＡ。结果表明：ＩＨＣ－７２对慢钙内流有直接抑制作用；其抑制触发性心律失常的机理与钙拮抗有关。
Using conventional glass microelectrode technique, we observed the slow response action potentials induced by depolarization of the membrane of the papillary muscle cells in the right 000 compartment of guinea pigs by 3,6- (dimethylamino) -benzodiazepine iodide cyclic edetate (IHC-72) (SAP), ouabain induced delayed depolarization (DAD) and triggering activity (TA). 2.54μMIHC-72 had no effect on the parameters of SAP; 25.4,101.6μMIHC-72 decreased the action potential amplitude (APA) by 7.4% and 19.3%, and the maximum increase rate of 0 phase (V_ ( max)) decreased by 2.5% and 39.1% respectively. The 100% action potential duration (APD_ (100)) of repolarization decreased by 7.1% and 41%, respectively. Effective refractory period (ERP) relative extended 4.9% and 9l. 3%, resting membrane potential (RMP) is not affected. The concentration of 25.4|ÌM HC-72 had no effect on the 50% action potential duration (APD 50) of repolarization, while APD 50 was shortened by 42.9% at the concentration of 101.6|ÌM, Dane-induced DAD and TA. The results showed that IHC-72 had a direct inhibitory effect on the influx of calcium and its mechanism of inhibition of triggering arrhythmia was related to calcium antagonism.