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兔冠状动脉结扎1小时缺血区心室肌细胞瞬间外向钾通道的变化
引用本文:齐书英,刘坤申,何振山,崔俊玉,杨丽,刘小云,张铁军.兔冠状动脉结扎1小时缺血区心室肌细胞瞬间外向钾通道的变化[J].中国心脏起搏与心电生理杂志,2003,17(4):287-290.
作者姓名:齐书英  刘坤申  何振山  崔俊玉  杨丽  刘小云  张铁军
作者单位:1. 白求恩国际和平医院心内科,河北石家庄,050082
2. 河北医科大学附属第一医院心内科
摘    要:为探讨在急性心肌梗死 (AMI)早期瞬间外向钾通道的变化及其在室性心律失常发生中的作用 ,以开胸冠状动脉 (简称冠脉 )结扎法制备兔急性心肌缺血模型 ,1h后处死动物分离心室肌细胞 ,采用全细胞膜片钳记录技术观察缺血区心外膜心室肌细胞瞬间外向钾通道电流 (Ito)的变化 ,以正常心肌Ito为对照。结果 :急性冠脉结扎 1h兔缺血区心室肌细胞Ito受到抑制 ,电流密度$C电压关系曲线下移 ,测试电压 + 60mV时的Ito电流密度对比显示 :对照组为 1 7.39± 5 .2 4pA/pF (n =1 2 ) ,冠脉结扎 1h组为 7.75± 3.1 1pA/pF (n =1 0 ) ,与对照组相比下降了 5 7% ,P <0 .0 0 1 ;其失活曲线左移 ,半数最大失活电压 (V1 /2 )对照组为 - 35 .2± 5 .3mV(n =1 2 ) ,冠脉结扎 1h组为 - 5 5 .1± 5 .6mV(n =1 0 ) ,与对照组比较失活速度加快 ,P <0 .0 1 ;冠脉结扎后 1h组Ito恢复明显减慢 ,恢复时程延长 ,P <0 .0 5。结论 :冠脉结扎后 1h缺血区心室肌细胞瞬间外向钾通道受抑制 ,影响动作电位复极 ,容易诱发 2相折返 ,可能为AMI后室性心律失常发生的机制之一。

关 键 词:电生理学    心肌梗死  急性  心肌细胞  膜片钳  瞬间外向钾电流
文章编号:1007-2659(2003)04-0287-04
修稿时间:2003年1月6日

Changes of Transient Outward Potassium Channel of Myocytes in Ischemic Zone of Rabbit Models 1 Hour after Coronary Artery Occlusion
QI Shu ying,LIU Kun shen,HE Zhen shan,et al..Changes of Transient Outward Potassium Channel of Myocytes in Ischemic Zone of Rabbit Models 1 Hour after Coronary Artery Occlusion[J].Chinese Journal of Cardiac Pacing and Electrophysiology,2003,17(4):287-290.
Authors:QI Shu ying  LIU Kun shen  HE Zhen shan  
Institution:QI Shu ying,LIU Kun shen,HE Zhen shan,et al.Department of Cardiology,Bethune International Peace Hospital,PLA,Shijiazhuang 0 5 0 0 82,Hebei,China
Abstract:To determine the changes of transient outward potassium currents(I to ) of rabbit ischemic myocytes after acute myocardial infarction(AMI). Rabbit models were made by ligation of branches of left coronary artery. After 1 hour, single ventricular myocytes were isolated enzymatically from ischemic zone, the normal cells from similar region in normal rabbit hearts. I to was recorded by using patch clamp techniques in the whole cell configuration. Results: I to at +60 mV from ischemic cells in the coronary occluded group was significantly reduced (7.75±3.11 pA/pF, n =10) compared to cells from control group (17.39±5.24 pA/pF, n =12), P <0.001, the I to density decreased 57%. The steady state inactivation curve was shifted to the hyperpolarizing direction in ischemic cells, the half maximal voltage dependence of inactivation(V 1/2 ) was -55.1±5.6 mV in ischemic cells and -35.2±5.3 mV in the control cells. Conclusion: Inhibitation of I to is found in the ischemic cells and might be important in the development of ventricular arrhythmias after AMI.
Keywords:Electrophysiology Rabbit  Myocardial infarction  acute Cardiomyocyte  Patch clamp Transient outward potassium current
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