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首页> 外文期刊>Cellular Physiology and Biochemistry >Inhibition of 2-aminoethoxydiphenyl borate-induced rat atrial ectopic activity by anti-arrhythmic drugs
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Inhibition of 2-aminoethoxydiphenyl borate-induced rat atrial ectopic activity by anti-arrhythmic drugs

机译：抗心律失常药抑制2-氨基乙氧基二苯基硼酸酯对大鼠心房异位活性的抑制

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Background/Aims: 2-aminoethoxydiphenyl borate (2-APB) provokes spontaneous mechanical activity in isolated rat left atria. The present study is to characterize 2-APB-induced ectopic activity in rat atria and to investigate the inhibition of 2-APB-induced ectopic activity by anti-arrhythmic drugs. Methods: 2-APB-induced ectopic activity was measured through an isometric force transducer connected to a multichannel acquisition and analysis system. Intracellular [Ca~2+]_i was measured with fluorescence laser scanning confocal microscopy. Voltage-dependent L-type Ca~(2+) currents were recorded by using patch-clamp technique. Results: 2-APB dose-dependently increased the ectopic activity of left atria at 1, 5, 10, 20, 50 μM. Anti-arrhythmic drugs, quinidine (10μM), lidocaine (10μM), verapamil (5μM), and amiodarone (50μM,100μM) inhibited 2-APB-induced ectopic activity. 2-APB-induced ectopic activity was inhibited by Ca~(2+)-free bath, Na~+/Ca~(2+) exchanger blockers, 3′,4′- dichlorobenzamil hydrochloride (DHC) and Ni~(2+), not by non-selective cation channel blocker Gd~(3+). 2-APB also induced ectopic contractions in ventricular tissue straps and the ectopic contractions were inhibited by quinidine, verapamil and DHC. Lidocaine, verapamil and DHC inhibited 2-APB-induced increase of intracellular Ca~(2+) concentration in cardiomyocytes. Low molecular weight heparin inhibited phenylephrine (PE)-induced but not 2-APB-induced atria ectopic activity, and the pattern of 2-APB-induced ectopic activity was continuous, distinct from the discontinuous activity induced by PE. Conclusion: 2-APB-induced atria ectopic activity was inhibited by classic anti-arrhythmic drugs quinidine, lidocaine, verapamil, amiodarone, and Na~(+), Ca~(2+) exchanger blockers. It can be used for testing agents able to affect any of Na~(+), Ca~(2+) channel, Na~(+)Ca~(2+) exchanger without selectivity.
机译：背景/目的：2-氨基乙氧基二苯基硼酸盐（2-APB）在离体大鼠左心房中引起自发的机械活动。本研究旨在表征2-APB诱导的大鼠心房异位活性，并研究抗心律失常药物对2-APB诱导的异位活性的抑制作用。方法：通过连接到多通道采集和分析系统的等距力传感器测量2-APB诱导的异位活性。用荧光激光扫描共聚焦显微镜测量细胞内[Ca〜2 +] _ i。采用膜片钳技术记录了电压依赖性的L型Ca〜（2+）电流。结果：2-APB剂量依赖性地增加了1、5、10、20、50μM时左心房的异位活性。抗心律失常药物奎尼丁（10μM），利多卡因（10μM），维拉帕米（5μM）和胺碘酮（50μM，100μM）抑制2-APB诱导的异位活性。 2-APB诱导的异位活性被无Ca〜（2+）浴，Na〜+ / Ca〜（2+）交换阻滞剂，3'，4'-盐酸二氯苯甲醚（DHC）和Ni〜（2+）抑制），而不是使用非选择性阳离子通道阻滞剂Gd〜（3+）。 2-APB还可诱发心室组织带的异位收缩，且异位收缩被奎尼丁，维拉帕米和DHC抑制。利多卡因，维拉帕米和DHC抑制2-APB诱导的心肌细胞内Ca〜（2+）浓度增加。低分子量肝素抑制苯肾上腺素（PE）诱导但不抑制2-APB诱导的心房异位活性，并且2-APB诱导的异位活性的模式是连续的，与PE诱导的间断活性不同。结论：经典抗心律不齐药物奎尼丁，利多卡因，维拉帕米，胺碘酮和Na〜（+），Ca〜（2+）交换阻断剂可抑制2-APB诱导的心房异位活性。它可以用于测试试剂，这些试剂能够影响Na〜（+），Ca〜（2+）通道，Na〜（+）Ca〜（2+）交换剂中的任何一种，而不会产生选择性。

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