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[1]贾冰,臧伟进. Ca2+在心肌缺血/再灌注损伤的线粒体调控机制中的作用[J]. 心脏杂志, 2007, 19(5):596-599.
[2]Marin-garcia J, Goldenthal MJ. Mitochondria play a critical role in cardioprotection[J]. J Card Fail, 2004, 10(1):55-66.
[3] Halestrap AP, Clarke SJ, Javadov SA. Mitochondrial permeability transition pore opening during myocardial reperfusion a target for cardioprotection[J]. Cardiovasc Res, 2004, 61(3):372-385.
[4]Shanmuganathan S, Hausenloy DJ, Duchen MR, et al. Mitochondrial permeability transition pore as a target for cardioprotection in the human heart[J]. Am J Physiol Heart Circ Physiol, 2005, 289(1):H237-H242.
[5]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.
[6] Zhao ZQ, Zang YM. Alternative cardioprotective stratrgy during reperfusion: postconditioning vs preconditioning[J].心脏杂志,2006,18(1):1-7,13.
[7]王凌,林荣. 缺血后适应对缺血/再灌注损伤的心肌保护[J]. 心脏杂志, 2007, 19(5):600-603,613.
[8]Nakagawa T, Shimizu S, Watanabe T, et al. Cyclophilin D-dependent mitochondrial permeability transition regulates somenecrotic but not apoptotic cell death[J]. Nature, 2005, 434(7033):652-658.
[9] Schneider MD. Cyclophilin D : Knocking on death's door[J]. Sci STKE, 2005, 2005(287):pe26.
[10]Basso E, Fante L, Fowlkes J, et al. Properties of the permeability transition pore in mitochondria devoid of cyclophilin D[J]. J Biol Chem, 2005, 280(19): l8558-l8561.
[11]Ruiz-meana M, Pina P, Garcia-dorado D, et al. Glycine protects cardiomyocytes against lethal reoxygenation injury by inhibiting mitochondrial permeability transition[J]. J Physiol, 2004, 558(3):873-882.
[12]Javadov SA, Clarke S, Das M, et al. Ischaemic preconditioning inhibits opening of mitochondrial permeability transition pores in the reperfused rat heart[J]. J Physiol, 2003, 549(Pt 2):513-524.