摘要
目的:检测慢性心力衰竭(CHF)大鼠心室肌钾电流的变化,探讨CHF时心律失常发生的可能机制。方法:建立腹主动脉缩窄大鼠CHF模型,采用全细胞膜片钳技术记录心室肌细胞短暂外向钾电流(Ito)、延迟整流性钾电流(IK)及内向整流性钾电流(IK1),并进行对照分析。结果:CHF组大鼠左心室收缩末压(LVSP)、左心室内压上升最大速率(+dp/dtmax)及左心室内压下降最大速率(-dp/dtmax)显著低于假手术组,左心室舒张末压(LVEDP)显著高于假手术组(均P<0.01),提示CHF模型制作成功。假手术组Ito的电流密度为(7.41±0.51)pA/pF,CHF组为(5.22±0.61)pA/pF,后者显著小于前者(P<0.01),Ⅰ～Ⅴ曲线显著下移;假手术组IK-tail的电流密度为(0.63±0.05)pA/pF,CHF组为(0.48±0.04)pA/pF,后者显著小于前者(P<0.01),Ⅰ～Ⅴ曲线显著下移;假手术组IK1内向电流密度为-(9.61±1.04)pA/pF,CHF组为-(6.33±0.71)pA/pF,后者显著小于前者(P<0.01),CHF组Ⅰ～Ⅴ曲线较假手术组显著上移。结论:CHF时,Ito、IK与IK1电流密度均显著减小,而IK和IK1减小可能是导致室性心律失常的重要原因。
Objective： To explore the changes of potassium ion currents in ventricular myocytes with chronic heart failure （CHF）. Method： Rat model of CHF of abdominal aortic banding was established. Whole ceil patch clamp technique was used to record transient outward potassium current （Ito）, delayed rectifying potassium cur- rent （IK）, inward rectifying potassium current （IK1）, and compared with pseudo-surgery group. Result：The left ventricular end-systolic pressure （LVSP）, the maximum increase rate of left ventricular pressure （ %- dp/dtmax ）, the maximum decrease rate of left ventricular pressure （- dp/dtmax ） of CHF group were significant lower than those of pseudo-surgery group （all P〈0.01）, the left ventricular end-diastolic pressure （LVEDP） of CHF group was significant higher than that of pseudo-surgery group （P〈0.01）. These data showed that the model was established successfully. The current density of Ito in CHF group was decreased significantly than that of pseudo- surgery group [（5.22±0.61）pA/pFvs （7.41±0.51）pA/pF, P〈0.011 and I -V curve was depressed. The current density of IK-tail in CHF group was decreased significantly than that of pseudo-surgery group [-（0.48± 0.04）pA/pFvs （0. 63±0. 05）pA/pF, P〈0.01] and I V curve was depressed. The current density of IK1 in CHF group was decreased significantly than that of pseudo-surgery group E--（6.33±0.71 ）pA/pF vs --（9.61± 0.04）pA/pF, P〈0. 011 and I V curve was upgrade. Conclusion：In CHF, the current density of Ito, IK and IK1 are all decreased significantly. The decrease of current density of IK.IK1 may play an important role in the development of ventrieular arrhythmia.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2012年第12期943-945,共3页
Journal of Clinical Cardiology
基金
国家973计划课题(No:2007CB512002)
国家自然科学基金项目(No:81270305)
国家科技支撑计划课题项目(No:2011BAI11B12)
关键词
心力衰竭
慢性
心室肌
钾电流
动物模型
chronic heart failure
ventricular myocyte
potassium ion currents
animal model
