活性氧在慢性缺氧性肺动脉高压发病机制中的作用  

Role of reactive oxygen species in pathogenesis of chronic hypoxic pulmonary arterial hypertension

作　　者：汤娜娜[1] 刘先胜[1] 徐永健[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院呼吸内科,武汉430030

出　　处：《国际呼吸杂志》2008年第5期318-320,共3页International Journal of Respiration

摘　　要：活性氧（reactive oxygen species，R0s）是肺血管系统内一种重要的信号传导分子。慢性缺氧使肺内动脉ROS生成增多，其主要来源是NAD（P）H氧化酶和（或）线粒体电子传递链。ROS的过度产生可引起肺动脉收缩反应和肺动脉结构重塑，在慢性缺氧性肺动脉高压的发生、发展中起重要作用。Reactive oxygen species （ROS） play important roles in signal transduction in pulmonary vasculatures. Chronic hypoxia increases ROS production from intrapulmonary artery. The source of increased ROS during chronic hypoxia is mediated primarily through NAD（P）H oxidase and/or the mitochondrial electron transport chain. The overproduction of ROS enhances intrapulmonary artery vasoconstrictor responsiveness and remodeling of pulmonary artery,both of which contribute to the pathogenesis of chronic hypoxic pulmonary arterial hypertension.

关 键 词：活性氧 慢性缺氧 肺动脉高压 

分 类 号：R544[医药卫生—心血管疾病]