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.