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吡那地尔后处理对缺血/再灌注大鼠离体心脏超微结构的影响 被引量:3

Effects of pinacidil postconditioning on myocardial ultrastructure of adult rats cardiac ischemia / reperfusion in vitro
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摘要 目的观察吡那地尔后处理对缺血/再灌注成年大鼠离体心脏超微结构和线粒体评分的影响。方法 24只健康雄性SD大鼠,采用Langendorff离体心脏灌流系统,建立缺血/再灌注损伤模型,随机分为4组(n=6),正常组(N)、缺血/再灌注组(I/R)、缺血后处理组(IPO)、吡那地尔后处理组(Pi),使用透射电子显微镜,观察各组心肌组织超微结构变化,并进行线粒体评分。结果电镜显示心肌细胞N组结构正常,I/R组损伤最严重,IPO组及Pi组损伤程度相似,介于N组与I/R组之间。N组、IPO组、Pi组线粒体评分均低于I/R组(P<0.05)。IPO组和Pi组线粒体评分无统计学意义(P=0.247)。结论缺血/再灌注可对心肌细胞超微结构造成严重损伤,使线粒体评分分值增加,造成心肌损害,缺血及吡那地尔后处理均可减轻再灌注所致心肌细胞超微结构损伤,降低线粒体评分分值,可能产生心肌保护作用。 Objective To observe the effects of pinacidil postconditioning on myocardial ultrastructure and mitochondria score in isolated heart ischemia / reperfusion of adult rats. Methods The hearts of adult healthy male Sprague- Dawley rats were isolated and subject to ischemia reperfusion injury. Hearts were randomly divided into four groups( n = 6 in each group) : Normal group( N),ischemia- reperfusion group( I / R),ischemic postconditioning group( IPO) and pinacidil postconditioning group( Pi). The ultrastructure and mitochondria score of myocardial tissue were observed by transmission electron microscope. Results Compared with those in I / R group,the damaged ultrastructure was attenuated and mitochondria score of myocardial cells were lower in IPO group and Pi group( P〈0. 05). No significant difference of mitochondria score of myocardial cells between IPO and Pi groups( P = 0. 247) was detected. Conclusion Ischemia / reperfusion could induce the damage of myocardial cell ultrastructure. IPO group and Pi group have similarly protective effects on myocardium from ischemia /reperfusion in isolated rat hearts.
出处 《遵义医学院学报》 2014年第6期595-597,共3页 Journal of Zunyi Medical University
基金 国家自然科学基金资助项目(NO:30960366)
关键词 吡那地尔后处理 缺血后处理 缺血/再灌注损伤 超微结构 心肌保护 pinacidil ischemic postconditioning ischemia / reperfusion injury ultrastructure myocardial protection
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  • 1赵淑敏,韩莉,马立辉,周健,孔祥玉.黄芪预处理对缺血再灌注大鼠心肌细胞凋亡及相关基因的影响(英文)[J].中国临床康复,2005,9(23):226-228. 被引量:15
  • 2Murry CE,Jennings RB,Reimer KA. Preconditioning with ischemia: A delay of lethal cell injury in ischemie myoeardium [J]. Circulation, 1986,74(5) :1124 - 1136. 被引量:1
  • 3Zhao 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. 被引量:1
  • 4Tissier R, Waintraub X, Couvreur N, et al. Pharmacological post conditioning with the phytoestrogen genistein [ J ] . J Mol Cell Cardiol,2007,42(1):79 - 87. 被引量:1
  • 5Yellon DM, Alkhulaifi AM, Browne EE, et al. Ischemie preconditioning limits infarct size in the rat heart [J]. Cardiovasc Res, 1992,26:983- 987. 被引量:1
  • 6Grover GJ, D' Alonzo AJ, Darbenzio RB, et al. In vivo characterization of the mitochondrial selective K(ATP) opener(3R)- trans- 4 - (4 - chlorophenyl)- N -( 1 H - imidazol - 2 - ylmethyl ) dimethyl - 2H - 1 - benzopyran - 6 - earbonitril monohydrochloride (BMS - 191095) :Cardioprotective, hemodynamic, and electrophysiological effects[J]. J Pharmacol Exp Ther, 2002,303 (1) : 132 - 140. 被引量:1
  • 7Feng J, Li H, Rosenkranz ER. K(ATP) channel opener protects neonatal rabbit heart better than thomas'solution[J]. J Surg Res,2003,109(2):69 -73. 被引量:1
  • 8Hausenloy DJ, Maddock HL, Baxter GF, et al. Inhibiting mitochondrial permeability transition pore opening: A new paradigm for myocardial preconditioning[J]. Cardioasc Res, 2002,55 : 534 - 543. 被引量:1
  • 9Hanley PJ, Mickel M, Loffer M, et al. K(ATP) channel - independent targets of diazoxide and 5 - hydroxydeeanoate in the heart [J]. J Physiol,2002,542(Pt 3) :735 - 741. 被引量:1
  • 10Holmuhamedov EL, Wang L, Terzic A. ATP - sensitive K^+ channel openers prevent Ca^2+ overload in rat cardiac mitochondria[J]. J Physiol, i999,519 (Pt2) : 347 - 360. 被引量:1

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