心力衰竭是许多疾病的终末阶段，心衰常常伴发心律失常，心衰期心源性猝死（SCD）的发生率大大增加。故揭示心衰病理过程中心律失常产生的机制，寻找有效的防治措施，是心血管领域研究的重要课题。研究表明钙调蛋白依赖激酶II（CaMKII）在心衰时表达增加，且过表达CaMKII可引起室性心律失常。为阐明在慢性心衰发病中CaMKII信号转导通路在室性心律失常中作用机制，我们将检测在慢性心衰大鼠心室中CaMKII和钾、钙离子通道的表达；采用膜片钳技术，观察慢性心衰大鼠心室肌细胞中钾、钙离子通道的电生理学特性改变；在以上基础上在整体和细胞水平探讨慢性心衰大鼠中心室CaMKII信号转导通路激活通过离子通道对室性心律失常的调节机制。本研究将揭示慢性心衰发病中CaMKII信号转导通路激活致钾、钙离子通道功能改变、室性心律失常发生机制，为慢性心衰室性心律失常的防治提供新的理论基础。

Heart failure (HF) is the end stage of many cardiovascular diseases. HF always accompanied with arrhythmia. Sudden cardiac death has high morbidity in HF. Although the drug therapy has make great progress in heart failure, the mortality is still very high. Therefore, the mechanism of arrhythmia is important to the treatment of HF. In order to elucidate the role of calcium/calmodulin-dependent protein kinase II (CaMKII) signal transduction pathway on the ventricular arrhythmia, the effect of CaMKII on ventricular arrhythmia through ion channel will be investigated in vivo. Patch clamp technique will be used to study the characteristic of ion channel. The effect of activation of CaMKII signal transduction pathway on the ion channel remodeling will be studied. Immunohistochemistry and molecular biology techniques will be used to study the expression of CaMKII signal transduction pathway activation and ion channels. The present study will elucidate the mechanism of ventricular arrhythmia mediated by CaMKII signal transduction pathway activation. It has important physiology and pathophysiologic significances in the prevention and therapy of SCD in HF.