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曲美他嗪后处理对大鼠心肌缺血再灌注损伤的保护性研究 被引量:7

Role of trimetazidine postconditioning in protecting rats against myocardial ischemia/reperfusion injury
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摘要 目的研究曲美他嗪后处理对大鼠急性心肌缺血再灌注后氧自由基损伤及细胞凋亡的影响。方法选择Wistar成年大鼠50只分为假手术组、再灌注损伤模型组(模型组)、曲美他嗪低剂量组(低剂量组)、曲美他嗪高剂量组(高剂量组)、缺血后处理组(后处理组),每组10只。后4组制作缺血再灌注损伤模型后,测定各组大鼠血流动力学变化,超氧化物歧化酶(SOD)、丙二醛水平,光镜、电镜下心肌组织切片观察。结果与假手术组比较,模型组、低剂量组、高剂量组和后处理组左心室舒张末压明显升高,左心室收缩压、左心室内压最大上升和下降速率明显减少(P<0.05,P<0.01)。与模型组比较,高剂量组、后处理组左心室舒张末压明显减低,左心室内压最大上升和下降速率明显增加(P<0.05)。与假手术组比较,模型组、低剂量组、高剂量组、后处理组丙二醛水平明显增高,SOD水平明显降低(P<0.05,P<0.01);与模型组比较,低、高剂量组、后处理组丙二醛水平明显减低,SOD水平明显升高(P<0.05,P<0.01)。结论高剂量曲美他嗪对大鼠心肌缺血再灌注损伤有保护作用。 Objective To study the effect of trimetazidine postconditioning on oxygen free radical jnjury and apoptosis in rats after acute myocardial I/R injury. Methods Fifty Wistar rats were randomly divided into sham operation group, reperfusion injury model group, low trimetazidine dose group, high trimetazidine dose group, and postconditioning group (10 in each group). A reperfusion injury model was established. The hemodynamics and serum SOD and MDA levels were measured. Myocardial tissue sections were observed under optical and electron microscope, respectively. Results The left ventricular end-diastolic pressure was significantly higher while the left ventricular systolic pressure and the maximal intraventricular pressure were significantly low- er in model group,high trimetazidine dose group, postconditioning group than in sham operation group and significantly lower in high trimetazidine dose group and postconditioning group than in in model group (P^0.01). The serum level of MDA was significantly higher while that of SOD was significantly lower in model group, low trimetazidine dose group, high trimetazidine dose group and postconditioning group than in sham operation group (P〈0.01). The serum level of MDA was significantly lower while that of SOD was significantly higher in low trimetazidine dose group, high trimetazidine dose group and postconditioning group than in model group (P〈0.01). Conclusion High trimetazidine dose can protect rats against myocardial I/R injury.
出处 《中华老年心脑血管病杂志》 CAS 北大核心 2014年第4期421-424,共4页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金 哈尔滨市科技局科技创新人才研究专项基金(2011RFQYS106)
关键词 曲美他嗪 心肌再灌注 活性氧 细胞凋亡 血流动力学 超氧化物歧化酶 丙二醛 trimetazidine myocardial reperfusion reactive oxygen species apoptosis hemodynam- ics superoxide dismutase malondialdehyde
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  • 1武毅,于晓风,曲绍春,睢大员.人参果皂苷对犬实验性心肌梗死的保护作用[J].中国药学杂志,2007,42(5):345-348. 被引量:37
  • 2赵新.实验性心肌缺血引起的脂质过氧化反应和抗氧化剂的抑制作用[J].西安医科大学学报,1987,2:133-133.
  • 3Brody GL, Belding WA, Belding M. The indentification and delineation of myocardial infarct[J]. Arch Pathol, 1967,B4: 312.
  • 4Pemow J. Endothelin in myocardial ischemia and reperfusion[ J ]. Cardiovasc Res, 1997,33(3) :518.
  • 5石湘云 姚松朝 杨哗.血管活性物质与临床[M].北京:北京医科大学中国协和医科大学联合出版社,1993.145-146.
  • 6Gill S, Haastrup B, Haghfelt T, Dellborg M, Clemmensen P. Continuous vectorcardiography is superior to standard electrocardiography in the prediction of long-term outcome after thrombolysis in patients with acute myocardial infarction. Coron Artery Dis 2002; 13: 169-75.
  • 7Krijnen PA. Nijmeijer R, Meijer CJ. Visser CA, Hack CE, Niessen HW. Apoptosis in myocardial ischemia and infarction. J Clin Pathol 2002; 55: 801-11.
  • 8Kumer D, Jugdutt BI. Apoptosis and oxidants in the heart. J Lab Clin Med 2003; 142: 288-97.
  • 9Cesselli D, Jakoniuk I, Barlucchi L, Beltrami AP, Hintze TH, Nadal-Ginard B, et al. Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy. Circ Res 2001; 89:279-86.
  • 10Kanoh M, Takemura G, Misao J, Hayakawa Y, Aoyama T, Nishigaki K, et al, Significance of myocytes with positive DNA in situ nick end-labeling (TUNEL) in hearts with dilated cardiomyopathy: not apoptosis but DNA repair. Circulation 1999; 99: 2757-64.

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  • 1桑文凤,桑桂梅,赵习德.曲美他嗪对老年缺血性心肌病患者缺血心肌的能量代谢及心脏功能的影响[J].中国老年学杂志,2014,34(4):915-917. 被引量:36
  • 2Sun Li-jun, Hao Yue-wen, Nie Xiao-wei, et al. Construction of PR39recombinant AAV under control of the HRE promoter and the effectof recombinant AAV on gene therapy of ischemic heart disease [J].Exp TherMed, 2012,4(5): 811-814.
  • 3Nishikimi T,Koichiro K, Nakagawa Y, et al. Adrenomedullin in car-diovascular disease: a useful biomarker, its pathological roles andtherapeutic application[J]. Curr Protein Pept Sci, 2013,14(4): 256-267.
  • 4Wong HK, Cheung TT, Cheung BM. Adrenomedullin and cardiovas-cular diseases[J]. JRSM Cardiovasc Dis, 2012, 1(5): 1-6.
  • 5Sun Li-jun, Hao Yue-wen, Nie Xiao-wei, et al. RecombinantAAV-PR39-mediated hypoxia-inducible factor 1 alpha gene expres-sion attenuates myocardial infarction [J]. Int J Mol Med, 2014,33(1):171-177.
  • 6Lichtenauer M, Mildner M, Baumgartner, et al. Intravenous and in-tramyocardial injection of apoptotic white blood cell suspensions pre-vents ventricular remodelling by increasing elastin expression in car-diac scar tissue after myocardial infarction [J]. Basic Res Cardiol,2011,106(4): 645-655.
  • 7Agnoletti G, Cargnoni A, Agnoletti L, et al. Experimental ischemiccardiomyopathy: insights into remodeling, physiological adaptation,and humoral response[J]. Ann Clin Lab Sci, 2006,36(3): 333-340.
  • 8Arai A E. Magnetic resonance imaging for area at risk, myocardial in-farction, and myocardial salvage [J]. J Cardiovasc Pharmacol Ther,2011,16(3-4):313-320.
  • 9Lee, PH, Ohtake T, Zaiou M, et al. Expression of an additional cathe-licidin antimicrobial peptide protects against bacterial skin infection[J]. Proc Natl Acad Sci USA,2005,102(10): 3750-3755.
  • 10Muinck,ED, Nagy N, Tirziu D, et al. Protection against myocardialischemia-reperfusion injury by the angiogenic Masterswitch proteinPR 39 gene therapy: the roles of HIF1 alpha stabilization and FGFR1signaling[J]. Antioxid Redox Signal, 2007, 9(4): 437-445.

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