一氧化氮合酶与心房颤动  

Nitric Oxide Synthase and Atrial Fibrillation

作　　者：俞菊梅[1] 李菊香[1] 

机构地区：[1]南昌大学第二附属医院心内科,南昌330006

出　　处：《国际老年医学杂志》2013年第6期269-272,共4页International Journal of Geriatrics

基　　金：国家自然科学基金项目（81060013）,江西省自然基金（2010GZY0254）

摘　　要：心房颤动（房颤）是临床上最常见的心律失常。研究证实，氧化应激参与房颤的发生发展，而房颤本身又加重氧化应激。氧化应激参与房颤发生的机制除与离子通道功能失调、NADPH氧化酶途径及线粒体损伤等有关外，大量证据表明其与一氧化氮合酶（NOS）密切相关。NOS是体内氧化剂来源之一，可催化一氧化氮（NO）合成，在特定条件下，NOS解偶联催化生成超氧化物阴离子，形成一种强大的自由基和氧化剂，从而促进房颤的发生与维持。Atrial fibrillation （AF） is the most common cardiac arrhythmia in clinical practice. The studies suggest that oxidative stress is involved in the development of atrial fibrillation, and atrial fibrillation itself also increases oxidative stress. The ion channel dysfunction, NADPH oxidase pathway and mitochondrial injury are all related to the mechanism of oxidative stress involved in atrial fi- brillation. And then many studies suggest it is also closely related to nitric oxide synthase （NOS）. NOS is one of the sources of oxidi- zing agents in vivo and under certain conditions it can synthesize nitric oxide （NO）. NOS uncoupling catalyzes the synthesis of superoxide anion and then becomes a strong radical and oxidant in order that it can contribute to the initiation and maintenance of atrial fibrillation .

关 键 词：房颤 氧化应激 一氧化氮合成酶 

分 类 号：R743.31[医药卫生—神经病学与精神病学]