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.
Key words:
Reactive oxygen species; Myocardial reperfusion injury; Mitochondria; Preconditioning; Postconditioning