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实验观察了ｌｅｍａｋａｌｉｍ（Ｌｅｍ）、ｐｉｎａｃｉｄｉｌ（Ｐｉｎ）、乙酰胆碱（Ａｃｈ）、ＴＩ＋及高Ｋ＋对小鼠心房肌早发后去极化（ＥＡＤ，由低Ｋ＋引起）的抑制作用。在Ｌｅｍ（２５μｍｏｌ／Ｌ）、Ｐｉｎ（８０μｍｏｌ／Ｌ）、Ａｃｈ（０．２μｍｏｌ／Ｌ）及ＴＩ＋（０．２ｍｍｏｌ／Ｌ）的作用下，心房肌动作电位时程（ＡＰＤ）呈不同程度缩短，而其他指标无变化。在Ｋ＋（５．０ｍｍｏｌ／Ｌ）的作用时，除ＡＰＤ缩短外，动作电位幅度及最大去极化速率也降低。用上述药物作用于ＥＡＤ时，Ａｃｈ及ＴＩ＋均可完全消除ＥＡＤ（分别为１０／１０及６／６）；Ｌｅｍ、Ｐｉｎ及Ｋ＋只在部分标本上完全消除ＥＡＤ（分别为８／９、３／１２及２／５）。虽然作用强度有差异，但上述钾通道激动剂（或开放剂）均对ＥＡＤ有抑制作用。
The inhibitory effects of lemakalim (Lem), pinacidil (Pin), acetylcholine (Ach), TI + and high K + on the depolarization (EAD, caused by low K + Under the action of Lem 25μmol / L, Pin 80μmol / L, Ach 0.2μmol / L and TI 0.2mmol / L, APD decreased to some extent, No change in other indicators. In the role of K + (5.0mmol / L), in addition to APD shortening, the action potential amplitude and maximum depolarization rate also decreased. EAD was completely abolished by both Ach and TI + with the above drugs (10/10 and 6/6, respectively); Lem, Pin and K + only partially eliminated EAD (8/9, 3/8, 12 and 2/5). Although the intensity of the difference, but the potassium channel agonists (or opener) are on EAD inhibition.