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［1］万晶晶，刘承云，成蓓.缺血预适应研究现状及展望［J］.心脏杂志，2006，18(4):465-466,471.

［2］臧益民，樊荣.加强多学科协作，争取心血管病研究取得新进展［J］.心脏杂志，2006，18(5):483-488.

［3］ Tsang A, Hausenloy DJ ,Mocanu MM, et al. Postconditioning: a form of“modified reperfusion”protects the myocardium by activating the phosphatidylinositol3kinaseAkt pathway［J］. Circ Res, 2004, 95(3): 230-232.

［4］ Zhao ZQ, Corvera JS, Halkos ME,et al.Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning［J］.Am J Physiol Heart Circ Physiol, 2003, 285(2): H579-H588.

［5］ Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia reperfusion injury by inhibiting events in the early minutes of reperfusion ［J］.Cardiovasc Res, 2004, 62(1): 74-85.

［6］ Philipp S,Downey JM, Cohen MV. Postconditioning must be initiated in less than 1 minute following reperfusion and is dependent on adenosine receptors and PI3kinase［J］. Circulation,2004,110(suppl Ⅰ):Ⅲ168.

［7］ Yang XM, Proctor JB, Cui L, et al. Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways［J］.J Am Coll Cardiol,2004, 44(5): 1103-1110.

［8］ Halkos ME, Kerendi F, Corvera JS,et al. Myocardial protection with postconditioning is not enhanced by ischemic preconditioning ［J］.Ann Thorac Surg,2004,78(3):961-969.

［9］ Galagudza M, Kurapeev D, Minasian S, et al.Ischemic postconditioning: brief ischemia during reperfusion converts persistent ventricular fibrillation into regular rhythm［J］.Eur J Cardiothorac Surg,2004,25(6):1006-1010.

［10］Sasaki H, Shimizu M, Ogawa K, et al.Brief IschemiaReperfusion Performed After Prolonged Ischemia (Ischemic Postconditioning) Can Terminate Reperfusion Arrhythmias With no Reduction of Cardiac Function in Rats［J］. Int Heart J, 2007,48（2）:205-213.

［11］Sun HY , Wang NP, Kerendi F, et al. Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload［J］.Am J Physiol Heart Circ Physiol,2005，288(4): H1900-H1908.

［12］Schwartz LM. Ischemic postconditioning during reperfusion fails to protect against lethal myocardial ischemiareperfusion injury in pigs［J］.Circulation,2004,110 ( suppl Ⅰ):Ⅲ106.

［13］Staat P, Rioufol G, Piot C,et al.Postconditioning the Human Heart［J］.Circulation,2005,112(14):2143-2148.

［14］马晓静，张兴华，罗曼，等.缺血预适应与缺血后适应现象对急性心肌梗死急症介入治疗后的影响［J］.中华医学杂志，2007,87（2）：114-117.

［15］Kerendi F,Kin H,Halkos ME, et al. Remote postconditioning. Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous activation of adenosine receptors［J］.Basic Res Cardiol, 2005,100（5）:404-412.

［16］李春梅,张兴华,马晓静,等.肢体缺血后处理对兔急性心肌缺血再灌注损伤的影响［J］.中国病理生理杂志,2006,22(12):2332-2335.

［17］李春梅,张兴华,马晓静,等.肢体缺血预处理和后处理对兔急性心肌缺血再灌注损伤的作用［J］.中华心血管病杂志,2006,34（12）：1138.

［18］Kin H, Lofye MT, Amerson BS,et al.Cardioprotection by“postconditioning”is mediated by increased retention of endogenous intravascular adenosine and activation of A2a receptors during reperfusion［J］. Circulation,2004,110(suppl Ⅰ):Ⅲ168.

［19］Krolikowski JG，Weihrauch D，Bienenbcaeber M，et al．Role of Erk l／2，p70s6K， and eNOS in isofluraneinduced cardiopmtection during early repefusion in vivo［J］．Can J Anaesth，2006，53(2)：174-182.

［20］Penna C, Mancardi D, Rastaldo R, et al. Intermittent activation of bradykinin B2 receptors and mitochondrial KATP channels trigger cardiac postconditioning through redox signaling［J］.Cardiovasc Res, 2007，75（1）：168-177.

［21］Halestrap AP, Clarke SJ, Javadov SAet al. Mitocbrondrial permeability transition pore opening during myocardial reperfusion a target for cardioprotection［J］.Cardiovasc Res,2004, 61(3): 372-385.

［22］Laurent Argaud, Odile GateauRoesch, Olivier Raisky,et al.Postconditioning Inhibits Mitochondrial Permeability Transition［J］.Circulation,2005,111（2）:194-197.

［23］Serviddio G,Di Venosa N，Federici A，et al. Brief hypoxia before normoxic reperfusion (postconditioning) protects the heart against ischemia reperfusion injury by preventing mitochondria peroxyde production and glutathione depletion［J］.FASEB J,2005,19（3）:354-361.

［24］Cohen MV, Yang XM, Downey JM. The pH hypothesis of postconditioning: staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosis［J］. Circulation,2007,115(14):1895-903.

［25］Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischemiareperfusion injury: targeting the reperfusion injury salvage kinase (RISK)pathway［J］. Cardiovasc Res，2004，61(3): 448-460.

［26］Zhao ZQ,VintenJohansen J. Postconditioning: reduction of reperfusioninduced injury［J］.Cardiovasc Res, 2006,70（2）:200-211.

［27］Zatta AJ, Kin H, Lee G, et al. Infarctsparing effect of myocardial postconditioning is dependent on protein kinase C signalling［J］.Cardiovasc Res, 2006,70（2）:315-324.

［28］VintenJohansen J,Yellon DM,Opie LH.Postconditioning:A Simple, Clinically Applicable Procedure to Improve Revascularization in Acute Myocardial Infarction［J］.Circulation,2005,112(14): 2085-2088.

［29］Iliodromitis EK, Zoga A, Vrettou A, et al. The effectiveness of postconditioning and preconditioning on infarct size in hypercholesterolemic and normal anesthetized rabbits［J］. Atherosclerosis, 2006,188（2）:356-362.

［30］Vanagt WY, Cornelussen RN, Baynham TC, et al. Pacinginduced dyssynchrony during early reperfusion reduces infarct size［J］.J Am Coll Cardiol, 2007,49（17）:1813-1819.

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