钾通道激动剂对小鼠心房肌早发后去极化的作用  

Effects of activators (or openers) of K^+ channels on early afterdepolarization of mouse atrial fibers

作　　者：陈希娟[1] 刘泰摓[1] 刘克球[1] 

机构地区：[1]北京大学生命科学学院生物膜与膜工程国家重点实验室

出　　处：《中华心血管病杂志》1995年第2期138-141,共4页Chinese Journal of Cardiology

摘　　要：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。Abstract Inhibitory effects of lemakalim (Lem), pinacidil (Pin),acetylcholine (Ach) , T1^+, and K^+ on early afterdepolarization (EAD) of mouse atrial fibers were observed.Under treatment with Lem (25μmol/L) , Pin ( 80 μmol/L), Ach ( 0. 2 μmol/L) or T1^+ (0. 2mmol/L)the durations of action potential (APD) of atrial fibers were reduced to different extents while other paraments of the action potential did not change significantly. Under K^+ (5. 0 mmol/L) superfusion, the amplitude of action potential and Vmax were also reduced together with APD. All of the these agents could inhibit EAD induced by low K^+ superfusion. Treatments with Ach and T1￣+ ,EADs were abolished completely (10/10 and 6/6, respectively) ,while with Lem , Pin and K￣+, EADs were abolished in some of the preparations (8/9 , 3/12 . and 2/5 respectively). It is suggested that activators of K￣+channels as well as inward current blockers, could inhibit EAD of mouse atrial fibers.

关 键 词：钾通道激动剂 心肌 早发后去极化 乙酰胆碱 

分 类 号：R965.2[医药卫生—药理学]