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中国临床药理学与治疗学 ›› 2010, Vol. 15 ›› Issue (2): 160-165.

• 基础研究 • 上一篇    下一篇

l-(2, 6-二甲基苯氧基)-2-(3, 4-二甲氧基苯乙氨基)丙烷盐酸盐对大鼠离体心脏缺血再灌注损伤的保护作用

张红霞, 吴勇杰, 高明堂   

  1. 兰州大学基础医学院药理学研究所,甘肃省新药临床前研究重点实验室,兰州 730000,甘肃
  • 收稿日期:2009-11-25 修回日期:2009-12-18 出版日期:2010-02-26 发布日期:2020-09-18
  • 通讯作者: 高明堂,男,博士,教授,硕士研究生导师,研究方向:心血管药理学。Tel: 13893150408 E-mail: gaomingtang@lzu.edu.cn
  • 作者简介:张红霞,女,硕士研究生,研究方向:心血管药理学。Tel: 13993141802 E-mail: wangtianya00@163.com
  • 基金资助:
    兰州大学医学基金项目(820619)

Protective effects of DDPH on myocardial ischemia reperfusion injury in isolated rat hearts

ZHANG Hong-xia, WU Yong-jie, GAO Ming-tang   

  1. Department of Pharmacology, School of Basic Medical Science of Lanzhou University, Key Laboratory of Preclinical Study of New Drugs of Gansu Province, Lanzhou 730000, Gansu, China
  • Received:2009-11-25 Revised:2009-12-18 Online:2010-02-26 Published:2020-09-18

摘要: 目的:研究l-(2, 6-二甲基苯氧基)-2-(3, 4-二甲氧基苯乙氨基) 丙烷盐酸盐(DDPH)对大鼠离体心脏缺血再灌注损伤的保护作用。方法:采用Langendorff大鼠离体心脏灌流技术,结扎冠状动脉前降支(LAD)40 min,复灌 120 min 后复制出大鼠离体心脏缺血再灌注损伤模型,观察DDPH对大鼠离体心脏左心室功能、心肌梗死范围、脂质过氧化及超微结构损伤的影响。结果:DDPH能显著改善大鼠离体心脏左心室功能,明显缩小心肌梗死范围,能显著提高大鼠心肌组织中超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,降低心肌脂质过氧化代谢产物丙二醛(MDA)含量,减少心肌超微结构损伤。结论:DDPH 对大鼠离体心脏缺血再灌注损伤有保护作用,其作用机制可能与抑制氧自由基的生成和脂质过氧化作用有关。

关键词: DDPH, 离体心脏灌流, 缺血再灌注损伤, 脂质过氧化

Abstract: AIM: To investigate the protective effect of 1-(2,6-dimethylphenoxy)-2-(3, 4-dimethoxyphenylethylamino) propane hydrochloride (DDPH) on myocardial ischemia-reperfusion (I/R) injury in isolated rat hearts. METHODS: Myocardial ischemia-reperfusion injury models were built with Langendorff isolated perfusion technology and established by the ligation of left descending coronary artery (LAD) for 40 min and reperfusion for 120 min in isolated rat hearts.The influence of DDPH on left ventricular function, myocardial infarct size, lipid peroxidation and the ultramicrostructural changes of myocardial cells were observed. RESULTS: DDPH improved the damage of left ventricular systolic and diastolic function caused by I/R, obviously reduced myocardial infarct size, increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), decreased the content of MDA in myocardium, and lessen the degree of ultramicrostructural injury in myocardial cells. CONCLUSION: DDPH has a protective effect on myocardial ischemia-reperfusion injury in isolated rat heart, which may be related to inhibiting the formation of the oxygen free radical and subsequent lipid peroxidation.

Key words: DDPH, Isolated heart perfusion, Ischemia-reperfusion injury, Lipid peroxidation

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