Nicorandil ameliorates impulse conduction disturbances during ischemia in isolated arterially perfused canine atria
Nicorandil ameliorates impulse conduction disturbances during ischemia in isolated arterially perfused canine atria
复制标题
DOI：
10.1016/j.ijcard.2009.06.011
复制
发表时间：
2011-01-07
影响因子：
3.5
通讯作者：
Yamada, Mitsuhiko
中科院分区：
文献类型：
--
作者：
Hirose, Masamichi;Yano, Shiharu;Yamada, Mitsuhiko
背景：尼可地尔对缺血性心房心肌有保护作用。然而，尼可地尔对缺血诱导的脉冲传导干扰的影响仍不确定。方法：记录左心房缺血时左心房256个部位的光学动作电位。从左上肺静脉（LSPV）和左后心房（PLA）进行恒定起搏（BCL=350 ms），计算LSPV-左心房（LA）交界处和右下PV (RIPV)-LA交界处的局部传导速度（CV）。在窦性心律的光学映射场中，脉冲传导失效。结果：在对照组中，无论起搏部位如何，缺血均减缓了这两个区域的局部CV，且窦性心律描记区内发生了脉冲传导失败。尼可地尔抑制了这两个区域的缺血传导减慢，防止了传导失败。尼可地尔还能减少局部缺血时CV的弥散。心脏肌层K-ATP通道阻滞剂HMR1098可消除尼可地尔对RIPV-LA连接处缺血传导减缓的抑制作用，而对LSPV-LA连接处则无抑制作用，并诱导传导失效。5-HD，一种线粒体K-ATP通道阻滞剂也在这两个区域消除了它并诱导了传导失败。5-HD消除了尼可地尔降低的局部CV弥散度，HMR1098与对照相比进一步增加了局部CV弥散度。结论：这些结果表明，尼可地尔通过作用于线粒体和肌层K-ATP通道来抑制缺血诱导的脉冲传导干扰。2009爱思唯尔爱尔兰有限公司版权所有。
Background: Nicorandil has protective effects on the ischemic atrial myocardium. However, effects of nicorandil on ischemia-induced impulse conduction disturbances are still uncertain.Methods: Optical action potentials were recorded from 256 sites of the left atrium in isolated arterially perfused canine atria during the left atrial ischemia. Constant pacing (BCL=350 ms) from the left superior pulmonary vein (LSPV) and the posterior left atrium (PLA) was performed, and local conduction velocity (CV) was calculated at the LSPV-left atrial (LA) junction and the right inferior PV (RIPV)-LA junction. Impulse conduction failure was elucidated within the optical mapping field during sinus rhythm.Results: In the control, ischemia slowed the local CV at both regions regardless of the pacing site, and impulse conduction failure occurred within the mapping field during sinus rhythm. Nicorandil suppressed the ischemic conduction slowing at both regions and prevented the conduction failure. Nicorandil also reduced the dispersion of local CV during ischemia. HMR1098, a blocker of cardiac sarcolemmal K-ATP channels abolished suppression of the ischemic conduction slowing by nicorandil at the RIPV-LA junction but not at the LSPV-LA junction and induced the conduction failure. 5-HD, a blocker of mitochondrial K-ATP channels also abolished it at both regions and induced the conduction failure. 5-HD abolished the decreased dispersion of local CV by nicorandil, and HMR1098 further increased the dispersion of local CV compared with the control.Conclusions: These results indicate that nicorandil suppresses ischemia-induced impulse conduction disturbances by its action on both the mitochondrial and sarcolemmal K-ATP channels. (C) 2009 Elsevier Ireland Ltd. All rights reserved.