期刊文献+

一氧化氮对心肌能量代谢影响的研究进展 被引量:1

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作者 崔彬 马捷
出处 《山西医科大学学报》 CAS 2001年第1期91-93,共3页 Journal of Shanxi Medical University
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参考文献22

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同被引文献13

  • 1郑关毅,陈晓春,刘昌云,方芳,张静,黄天文,曾育琦.一氧化氮激活应激活化蛋白激酶/c-Jun氨基末端激酶及p38MAP激酶诱导脑缺血再灌注后神经元凋亡[J].解剖学报,2006,37(6):633-639. 被引量:4
  • 2齐娜,廖迎,张贵林.心肌缺血再灌注损伤及药物治疗研究进展[J].华夏医学,2007,20(1):170-172. 被引量:8
  • 3Schulze - Osthoff K, Bauer MK, Vogt M, et al. Oxidative stress and signal transduction [J]. Int J Vitam Nutr Res, 1997,67 (5) : 336 - 342.
  • 4Qi SH, Hao LY, Yue J, et al. Exogenous nitric oxide negativelyregulates the S - nitrosylation p38 mitogen - activated protein ki- nase activation during cerebral ischaemia and reperfusion [ J ]. Neuropathol Appl Neurebiol, 2013,39 (3) :284 - 297.
  • 5Liu DH, Yuan FG, Hu SQ, et al. Endogenous nitric oxide in- duces activation of apoptosis signal - regulating kinase 1 via S - nitrosylation in rathippocampus during cerebral isehemia - reperfu- sion [ J ]. Neuroscience, 2013,229:36 - 48.
  • 6Bhushan S, Kondo K, Predmore BL, et al. Selective q3 - adreno- receptor stimulation attenuates myocardial cell death and preserves cardiac function after ischemia - reperfusion injury [ J ]. Arterio- scler Thromb Vasc Biol, 2012,32(8) :1865 - 1874.
  • 7Zhao ZQ, Vinten - Johansen J. Myocardial apoptosis and ischemic preconditioning [ J ]. Cardiovasc Res, 2002,55 ( 3 ) :438 - 455.
  • 8Ma XL, Kumar S, Gao F, et al. Inhibition of p38 mitogen - acti- vated protein kinase decreases cardiomyocyte apoptosis and im- proves cardiacfunction after myocardial ischemia and reperfusion [ J]. Circulation, 1999,99 (13) : 1685 - 1691.
  • 9Ferrandi C, Ballerio R, Gaillard P, et al. Inhibition of c - Jun N -terminal kinase decreases cardiomyocyte apoptosis and infarct size after myocardial ischemia and reperfusion in anaesthetized rats [J]. Br J Pharmacol, 2004,142(6) :953 -960.
  • 10郑波,张奇惠,李跃荣.心肌缺血再灌注损伤机制研究进展[J].滨州医学院学报,2008,31(2):121-123. 被引量:21

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