国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2010年
3期
233-236
,共4页
活性氧%心肌再灌注损伤%线粒体%预处理%后处理
活性氧%心肌再灌註損傷%線粒體%預處理%後處理
활성양%심기재관주손상%선립체%예처리%후처리
Reactive oxygen species%Myocardial reperfusion injury%Mitochondria%Preconditioning%Postconditioning
既往认为在心肌缺血/再灌注过程中活性氧是一种有害的细胞损伤因子,但最近研究发现也是可产生细胞保护作用的信号分子.活性氧(reactive oxygen species,ROS)在缺血,再灌注及其内源性心肌保护作用中具有双重作用,内源性心肌保护过程中活性氧主要来自线粒体呼吸链,主要通过mKATP-ROS通路产生;活性氧通过改变细胞氧化还原状态和调节线粒体膜通透性转换孔道开放状态,传递线粒体和细胞之间的信息联系.因此.活性氧不单是缺血/再灌注氧化应激的损伤因子,也是产生内源性心肌保护作用的重要信号分子.
既往認為在心肌缺血/再灌註過程中活性氧是一種有害的細胞損傷因子,但最近研究髮現也是可產生細胞保護作用的信號分子.活性氧(reactive oxygen species,ROS)在缺血,再灌註及其內源性心肌保護作用中具有雙重作用,內源性心肌保護過程中活性氧主要來自線粒體呼吸鏈,主要通過mKATP-ROS通路產生;活性氧通過改變細胞氧化還原狀態和調節線粒體膜通透性轉換孔道開放狀態,傳遞線粒體和細胞之間的信息聯繫.因此.活性氧不單是缺血/再灌註氧化應激的損傷因子,也是產生內源性心肌保護作用的重要信號分子.
기왕인위재심기결혈/재관주과정중활성양시일충유해적세포손상인자,단최근연구발현야시가산생세포보호작용적신호분자.활성양(reactive oxygen species,ROS)재결혈,재관주급기내원성심기보호작용중구유쌍중작용,내원성심기보호과정중활성양주요래자선립체호흡련,주요통과mKATP-ROS통로산생;활성양통과개변세포양화환원상태화조절선립체막통투성전환공도개방상태,전체선립체화세포지간적신식련계.인차.활성양불단시결혈/재관주양화응격적손상인자,야시산생내원성심기보호작용적중요신호분자.
In recent years the main idea has been that reactive oxygen species (ROS) play an essential,though double-edged, role in cardioprotection: they may participate in reperfusion injury or may play a role as signaling elements during myocardial adaptation to ischemia. It has been demonstrated that pre-or postconditioning triggering is redox-sensitive, via a mitochondrial KATP-ROS-dependent mechanism.In these cardioprotective phenomenon a redox signal and inhibition of mPTP are required during myocardial reperfusion following the index ischemic period. Therefore, the role of ROS in reperfusion may be reconsidered as they are not only deleterious.
