The role of reactive oxygen species and redoxsensitive protein kinases in the infarction-limiting effect of opioid peptide deltorphin II in cardiac reperfusion in rats

Background. Mortality from acute myocardial infarction with ST-segment elevation in cardiac hospitals ranges 4.5 to 7 %, and these data has not decreased recent years. The most common cause of death patients is cardiogenic shock, the likelihood which directly depends on infarct size. It quite clear that there an urgent need create drugs limit size prevent occurrence shock. aim. To evaluate role reactive oxygen species redox-sensitive protein kinases infarction-limiting effect opioid peptide deltorphin II reperfusion rats. Materials methods. Coronary occlusion (45 min) (120 were performed rats anesthetized α-chloralose. selective δ 2 -opioid receptor agonist II, a hydroxyl radical scavenger 2-mercaptoprpionyl glycine (2-MPG), superoxide tempol, kinase Cδ (PKCδ) inhibitor rottlerin, PI3-kinase wortmannin, ERK1/2 PD98059 injected before heart. Results. Deltorphin contributed two-fold decrease Injection 2-MPG, alone had no 2-MPG tempol did affect infarction-reducing II. Rottlerin, eliminated cardioprotective Conclusion. does depend production radical. Superoxide do play significant injury heart after coronary min). PKCδ, PI3-kinase, are involved reperfusion.