Myocardial protection after adaptation Progress.doc

 PAGE \* MERGEFORMAT 18 Myocardial protection after adaptation Progress [Keywords:], after adaptation, myocardial protection, reperfusion injury salvage kinase, review [publication type] Effective in restoring early coronary blood flow obstruction is to reduce myocardial infarct size and improve the prognosis of patients the most effective treatment measures, but their induction of lethal reperfusion injury, including apoptosis or necrosis, can account for the final infarct size of 50 % [1]. Murry et al [2], ischemic preconditioning (IPC methods to improve organ of continuous ischemia and reperfusion injury tolerance, but acute myocardial infarction (AMI unpredictability of events limits the IPC in the clinical In 2003 the practice of the application, Zhao et al [3], left anterior descending artery occlusion in dogs 60 min after reperfusion began immediately to 3 times turn of reperfusion / ischemia in operation, reducing the infarct. This leads to the ischemic postconditioning (IPost concepts: persistent ischemia in the organ during early reperfusion, and IPC sub damage similar to reperfusion / ischemia can induce organ protection. research suggests IPost and IPC are similar in signal transduction mechanisms, including reperfusion injury salvage kinase (RISK pathway activation and mitochondrial permeability transition pore (mPTP opening inhibition [4]. authors IPost and drugs associated with adaptation (PPost and distant organs after the adaptation (RPost at Research Progress in myocardial protection are reviewed. 1 to the endogenous protective mechanisms of adaptation: RISK activation pathway 1.1 G protein-coupled receptor (GPCR activation GPCR is a class of cell surface transmembrane receptor proteins involved in the process of extracellular signal incoming. IPost induced by adenosine, opioids, bradykinin, and other endogenous signaling molecules, by ligand by way of binding activated GPCR, activating its intracellular tyrosine kinase, causing a