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|本期目录/Table of Contents|

迷走神经在心律失常发生中的研究进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第5期
页码:
646-650
栏目:
综述
出版日期:
2012-10-25

文章信息/Info

Title:
Role of vagal nerve in cardiac arrhythmia
作者:
冯 璇臧伟进周 筠
(西安交通大学医学院药理学系,陕西 西安 710061)
Author(s):
FENG Xuan ZANG Wei-jin ZHOU Jun
(Department of Pharmacology, College of Medicine, Xi’an Jiaotong University, Xi’an 710061, Shaanxi, China)
关键词:
长QT综合征迷走神经心律失常
Keywords:
Long QT syndrome vagal nerve cardiac arrhythmia
分类号:
R541.7
DOI:
-
文献标识码:
A
摘要:
作为遗传性心律失常之一的长QT综合征(LQTS),现已发现有12型,其中在中国以LQT2为常见,可诱发尖端扭转型室性心动过速及室颤,临床上以反复发作的晕厥及常导致的猝死为特征。自主神经通过释放神经递质作用于受体调节离子通道,从而对某些心律失常起到一定的作用,而迷走神经通过直接或间接作用对多种心律失常具有一定的保护作用。本文主要对LQT2的研究进展、迷走神经与LQT2的关系以及其在心律失常中发挥的作用作一综述。
Abstract:
As one of the familial abnormalities of cardiac rhythm, Long QT syndrome (LQTS) has been found in 12 different genes. LQT2 is one of the most common LQTS in China, which can lead to Torsade de Points (TdP) and ventricular fibrillation (VF). Clinically it is characterized by recurrent syncope and sudden cardiac death. The autonomic nervous system plays a vital role in some cases of cardiac arrhythmia through the release of neurotransmitter to regulate ion channel. Recently, studies have shown that vagal nerve can reduce the occurrence of certain kinds of cardiac arrhythmia and may play an important role in maintaining normal cardiac rhythm and rate. This paper mainly reviews the recent advances of LQT2, the complex relationship between vagal nerve and LQT2, and the role of vagal nerve in cardiac arrhythmia.

参考文献/References

[1]范丹丹,周 筠.LQT2相关HERG基因的功能和表达[J].心脏杂志,2012,24(3):402-406.
[2]胡 丹,阮 磊,张存泰,等.先天性长QT综合征新进展[J].中国心脏起搏与心电生理杂志,2011,25(5):378.
[3]Sroubek J,McDonald TV.Protein Kinase A activity at the endoplasmic reticulum surface is responsible for augmentation of human ether-a-go-go-related gene product (HERG)[J].J Biol Chem,2011,286(24):21927-21936.
[4]Harmati G,Papp F,Szentandrássy N,et al.Effects of the PKC inhibitors chelerythrine and bisindolylmaleimide I (GF 109203X) on delayed rectifier K+ currents[J].Naunyn-Schmiedebergs Arch Pharmacol,2011,383(2):141-148.
[5]Ilanit I,Leonid M, Irit H,et al.Modelling the long QT syndrome with induced pluripotent stem cells[J].Nature,2011, 471(7337):225-U113.
[6]Lahti AL,Kujala VJ,Chapman H,et al.Model for long QT syndrome type 2 using human iPS cells demonstrates arrhythmogenic characteristics in cell culture[J].Dis Model Mech, 2012,5(2):220-230.
[7]Quan XQ,Bai R,Lu JG,et al.Pharmacological Enhancement of Cardiac Gap Junction Coupling Prevents Arrhythmias in Canine LQT2 Model[J].Cell Commun Adhes,2009,16(1-3):29-38.
[8]Němec J,Kim JJ,Gabris B,et al.Calcium oscillations and T-wave lability precede ventricular arrhythmias in acquired long QT type 2[J].Heart Rhythm,2011,7(11):1686-1694.
[9]Milberg P,Frommeyer G,Kleideiter A,et al.Antiarrhythmic effects of free polyunsaturated fatty acids in an experimental model of LQT2 and LQT3 due to suppression of early afterdepolarizations and reduction of spatial and temporal dispersion of repolarization[J].Heart Rhythm,2011,8(9):1492-1500.
[10]Liu GX,Choi BR,Ziv O,et al.Differential conditions for early after-depolarizations and triggered activity in cardiomyocytes derived from transgenic LQT1 and LQT2 rabbits[J].J Physiol-London,2012,590(Pt5):1171-1180.
[11]Odening KE,Kirk M,Brunner M, et al.Electrophysiological studies of transgenic long QT type 1 and type 2 rabbits reveal genotype-specific differences in ventricular refractoriness and His conduction[J].Am J Physiol-Heart Circul Physiol,2010,299(3):H643-H655.
[12]Wang S,Xu DJ,Cai JB,et al.Rapid component I(Kr) of cardiac delayed rectifier potassium currents in guinea-pig is inhibited by alpha(1)-adrenoreceptor activation via protein kinase A and protein kinase C-dependent pathways[J].Eur J Pharmacol,2009,608(1-3):1-6.
[13]Chen J,Chen K,Jakub S,et al.Post-transcriptional control of human ether-a-go-go-related gene potassium channel protein by alpha-adrenergic receptor stimulation[J].Mol Pharmacol,2010,78(2):186-197.
[14]Goldenberg I,Bradley J,Moss A,et al. Beta-blocker efficacy in high-risk patients with the congenital long-QT syndrome types 1 and 2: implications for patient management[J].J Cardiovasc Electrophysiol,2010,21 (8):893-902.
[15]van Borren MM,Verkerk AO,Wilders R,et al.Effects of muscarinic receptor stimulation on Ca2+ transient, cAMP production and pacemaker frequency of rabbit sinoatrial node cells[J].Basic Res Cardiol,2010,105(1):73-87.
[16]Clark AJ,Kuperman RA,Auguste KI,et al.Intractable episodic bradycardia resulting from progressive lead traction in an epileptic child with a vagus nerve stimulator:a delayed complication Case report[J].J Neurosurg-Pediatr,2012,9(4):389-393.
[17]Oliveira M,da Silva MN,Geraldes V,et al.Acute vagal modulation of electrophysiology of the atrial and pulmonary veins increases vulnerability to atrial fibrillation[J].Exp Physiol,2011,96(2):125-133.
[18]Zhang Y,Ilsar I,Sabbah HN,et al.Relationship between right cervical vagus nerve stimulation and atrial fibrillation inducibility: therapeutic intensities do not increase arrhythmogenesis[J].Heart Rhythm,2009,6(2):244-250.
[19]Sheng X,Scherlag BJ,Yu L, et al. Prevention and reversal of atrial fibrillation inducibility and autonomic remodeling by low level vagosympathetic nerve stimulation[J].J Am Coil Cardiol,2011,57(5):563-571.
[20]Igarashi T,Finet JE,Takeuchi A,et al.Connexin gene transfer preserves conduction velocity and prevents atrial fibrillation[J].Circulation,2012,125(2):216-215.
[21]Zhang YH,Todor N.Arrhythmias and vagus nerve stimulation[J].Heart Fail Rev,2011,16(2):147-161.
[22]Ng GA,Brack KE,Patel VH,et al.Autonomic modulation of electrical restitution, alternans and ventricular fibrillation initiation in the isolated heart[J].Cardiovasc Res,2007,73(4):750-760.
[23]Brack KE,Patel VH,Coote JH,et al.Nitric oxide mediates the vagal protective effect on ventricular fibrillation via effects on action potential duration restitution in the rabbit heart[J].J Physiol,2007,583(2):695-704.
[24]Wu W,Li Y,Lu Z.Increased susceptibility to ischemia-induced ventricular tachyarrhythmias in depressed rats:Involvement of reduction of connexin 43[J].Exp Ther Med,2012,3(2):192-194.

备注/Memo

备注/Memo:
收稿日期:2012-04-21.
基金项目:国家自然科学基金项目资助(30930105,81170176); 西安交通大学自主创新项目资助(XJJ20100036)
通讯作者:周筠,副教授,主要从事心血管药理学研究Email:jzhou829@yahoo.com.cn
作者简介:冯璇,硕士生Email:fengxuan0723@163.com
更新日期/Last Update: 2012-11-16