心力衰竭中心室肌细胞的离子通道重构与电活动的稳态调节  

Remodeling and homeostasis of ion channels in ventricular myocytes in heart failure

作　　者：宁菲菲[1] 杨丹丹[1] 白鸿远[1] 马爱群[1] 

机构地区：[1]西安交通大学医学院第一附属医院心血管内科 教育部环境与基因相关疾病重点实验室/心血管离子通道病研究室,西安710061

出　　处：《中国医学前沿杂志（电子版）》2013年第9期30-35,共6页Chinese Journal of the Frontiers of Medical Science(Electronic Version)

基　　金：国家自然科学基金(30830051)

摘　　要：心力衰竭是多种心血管疾病的最终结局。心力衰竭时存在心脏器官水平的结构重构和细胞、离子通道分子水平的心电重构。心脏的离子通道重构最初是在病理状态下维持心功能的适应性反应,但持续存在的病理状态导致的重构本身也可以引起疾病的发生,与心力衰竭中心律失常的发生密切相关。心力衰竭时心室肌细胞多种离子通道的表达和功能发生变化,如IK1、Ito、IKs、ICa-L、IK、INaL、INa+/Ca2+等,导致心室肌细胞的静息电位和动作电位的各期均发生从细微到显著的变化,存在离子通道的重构与心肌细胞电活动的稳态调节。从整体上逆转离子通道重构,以所有离子通道的稳态调节为目标进行治疗,可能是改善心力衰竭时心电重构的关键。Heart failure (HF) is the ifnal ending of a variety of cardiovascular diseases. There is not only the structural remodeling in heart but also electrical remodeling in the ion channels. Remodeling of the ion channels, which is adaptive response to preserve cardiac function under pathological stress initially, leads to dysfunction itself if the stress is maintained and it is closely related to arrhythmias in HF. Many ion channels of ventricular myocytes change their expressions and functions in HF, such as IK1, Ito, IKs, ICa-L, IK, INaL, INa+/Ca2+, and so on. The resting potential and every period of action potential have their remodeling and homeostasis regulation of ion channels in ventricular myocytes. It provides us a new perspective that reversing the remodeling of ion channels as a whole and regulate the homeostasis of all ion channels is the key to improve the electrical remodeling in HF.

关 键 词：心力衰竭 离子通道 稳态调节 心律失常 

分 类 号：R541.6[医药卫生—心血管疾病]