抗心律失常药物对2-APB诱发大鼠心房异位活动的影响

Inhibition of 2-aminoethoxydiphenyl-borate-induced rat atrial ectopic activity by antiarrhythmic drugs

目的研究抗心律失常药物对2-APB诱发的大鼠心房异位活动的抑制作用。方法通过连接多通道分析和获取数据的等长张力传感器测量2-APB诱发的异位活动。结果 2-APB剂量依赖性增加左心房的异位活动,浓度分别为1、5、10、20、50μmol·L^(-1)。抗心律失常药物,奎尼丁(10μmol·L^(-1)),利多卡因(10μmol·L^(-1)),维拉帕米(5μmol·L^(-1))抑制2-APB诱发的异位活动。2-APB诱发的异位活动能被无钙液和Na^+/Ca^(2+)交换抑制剂所阻断,如3',4'-dichlorobenzamil hydrochloride(DHC)和Ni^(2+),而不能被非选择性阳离子通道阻断剂Gd^(3+)所阻断。结论 2-APB诱发的心房异位活动能被经典抗心律失常药物所抑制,如奎尼丁,利多卡因,维拉帕米和钠钙交换抑制剂。2-APB可用于筛选那些能够非选择性抑制钠通道,钙通道和钠钙交换体的抗心律失常药物。

Objective To explore the inhibition of 2-APB-induced rat atrial ectopic activity by antiarrhythmic drugs. Methods 2-APB-induced ectopic activity was measured through an isometric force transducer connected to amultichannel acquisition and analysis system. Results 2-APB dose-dependence increased the ectopic activity of left atria at 1,5,10,20,50 μmol·L^(-1). Anti-arrhythmic drugs,quinidine( 10 μmol·L^(-1)),lidocaine( 10 μmol·L-1),verapamil( 5 μmol·L^(-1)) inhibited 2-APB-induced ectopic activity. 2-APB-induced ectopic activity was inhibited by Ca2 +-free bath,Na+/ Ca^(2+)exchanger blockers,3 ',4 '-dichlorobenzamil hydrochloride( DHC) and Ni^(2+),not by non-selective cation channel blocker Gd^(3+). Conclusions 2-APB-induced atrial ectopic activity was inhibited by classic anti-arrhythmic drugs quinidine,lidocaine,verapamil,and Na+/ Ca2 +exchanger blockers. It can be used for testing agents able to affect any of Na^+,Ca^(2+)channel,Na^+/Ca^(2+) exchanger without selectivity.