“…On the other hand, reperfusion leads to further cardiomyocyte injury (lethal reperfusion injury), with effects ranging from activation of ROS to increases in Ca 2+ overload or stimulation of the inflammatory cascade and can have deleterious effects on the already injured myocardium [56,57]. The main culprits of this action are believed to be the leukocytes [58], as well as endothelial cells that are activated by various proinflammatory cytokines (IL-6, IL-8, TNF-α) and the complement system (C5a/C5b mainly) [59]. Lastly, various adaptations of the I/R protocol have been investigated (involving pre-and post-conditioning) and have shown to protect from the I/R injury, with anti-inflammatory effects forming the basis of this protective action.…”