Intermittent high altitude hypoxia inhibits opening of mitochondrial permeability transition pores against reperfusion injury
作者： Wei-Zhong Zhu , Yan Xie , Le Chen , Huang-Tian Yang , Zhao-Nian Zhou
DOI: 10.1016/J.YJMCC.2005.09.016
关键词:
摘要: The role of mitochondrial permeability transition pore (MPTP) in the mechanism intermittent high altitude (IHA) hypoxic adaptation is not understood. Therefore, we study whether protective effect IHA hypoxia against ischemia-reperfusion injury accompanied by inhibition MPTP opening. significantly improved functional recovery Langendorff hearts on reperfusion and limited infarct size. In isolated myocytes, cell length, lowered ischemia-reperfusion-induced [Ca2+]c [Ca2+]m overloading. Furthermore, accelerated decline during reperfusion. Opening with atractyloside immediately at abolished these cardioprotective effects hypoxia, but had no appreciable influence those normoxic hearts. prolongs time taken to induce opening rigor contracture when myocytes subjected oxidative stress. data from mitochondria demonstrated that prevented decrease ADP/O ratio, release cytochrome c Ca2+ concentrations (100 200 microM). Inhibition first few minutes attenuated overloading, which contributed cardioprotection adaptation. Enhancement tolerance might underlie hypoxia.
elsevier.com
jmmc-online.com 参考文章(38)
Fabio Di Lisa, Paolo Bernardi, Mitochondrial function as a determinant of recovery or death in cell response to injury Bioenergetics of the Cell: Quantitative Aspects. ,vol. 184, pp. 379- 391 ,(1998) , 10.1007/978-1-4615-5653-4_25
A. P. Halestrap, C. P. Connern, E. J. Griffiths, P. M. Kerr, Cyclosporin A binding to mitochondrial cyclophilin inhibits the permeability transition pore and protects hearts from ischaemia/reperfusion injury Molecular and Cellular Biochemistry. ,vol. 174, pp. 167- 172 ,(1997) , 10.1007/978-1-4615-6111-8_25
Derek J Hausenloy, Michael R Duchen, Derek M Yellon, Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia–reperfusion injury Cardiovascular Research. ,vol. 60, pp. 617- 625 ,(2003) , 10.1016/J.CARDIORES.2003.09.025
FelixZ. Meerson, IgorYu. Malyshev, AlexanderV. Zamotrinsky, Differences in adaptive stabilization of structures in response to stress and hypoxia relate with the accumulation of hsp70 isoforms. Molecular and Cellular Biochemistry. ,vol. 111, pp. 87- 95 ,(1992) , 10.1007/BF00229578
Sabzali A Javadov, Samantha Clarke, Manika Das, Elinor J Griffiths, Kelvin HH Lim, Andrew P Halestrap, None, Ischaemic preconditioning inhibits opening of mitochondrial permeability transition pores in the reperfused rat heart The Journal of Physiology. ,vol. 549, pp. 513- 524 ,(2003) , 10.1113/JPHYSIOL.2003.034231
Yi Zhang, Ning Zhong, Zhao-Nian Zhou, Effects of intermittent hypoxia on action potential and contraction in non-ischemic and ischemic rat papillary muscle. Life Sciences. ,vol. 67, pp. 2465- 2471 ,(2000) , 10.1016/S0024-3205(00)00832-8
Derek J. Hausenloy, Derek M. Yellon, Siva Mani-Babu, Michael R. Duchen, Preconditioning protects by inhibiting the mitochondrial permeability transition American Journal of Physiology-heart and Circulatory Physiology. ,vol. 287, pp. 841- 849 ,(2004) , 10.1152/AJPHEART.00678.2003
Yan Xie, Wei-Zhong Zhu, Yi Zhu, Le Chen, Zhao-Nian Zhou, Huang-Tian Yang, Intermittent high altitude hypoxia protects the heart against lethal Ca2+ overload injury Life Sciences. ,vol. 76, pp. 559- 572 ,(2004) , 10.1016/J.LFS.2004.09.017
Andrew P. Halestrap, Paul M. Kerr, Sabzali Javadov, K.-Y. Woodfield, Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart Biochimica et Biophysica Acta. ,vol. 1366, pp. 79- 94 ,(1998) , 10.1016/S0005-2728(98)00122-4
Hai-Feng Zhu, Jian-Wen Dong, Wei-Zhong Zhu, Hai-Lei Ding, Zhao-Nian Zhou, ATP-dependent potassium channels involved in the cardiac protection induced by intermittent hypoxia against ischemia/reperfusion injury Life Sciences. ,vol. 73, pp. 1275- 1287 ,(2003) , 10.1016/S0024-3205(03)00429-6