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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。
AIM: To investigate the effects of l- (2,6-dimethylphenoxy) -2- (3,4-dimethoxyphenethylamino) propane hydrochloride (DDPH) on isolated rat heart ischemia- Injury protection. Methods: Langendorff rat heart was perfused with LAD and ligated with LAD for 40 min. After reperfusion for 120 min, the model of isolated rat heart ischemia-reperfusion injury was established. The effects of DDPH on rat isolated Left ventricular function, myocardial infarct size, lipid peroxidation and ultrastructural damage. RESULTS: DDPH could significantly improve left ventricular function in isolated rat hearts and significantly reduce the extent of myocardial infarction. It could significantly increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) Activity, reduce myocardial lipid peroxidation metabolites malondialdehyde (MDA) content, reduce myocardial ultrastructure damage. CONCLUSION: DDPH has a protective effect on ischemia-reperfusion injury in isolated rat hearts and its mechanism may be related to the inhibition of the production of oxygen free radicals and lipid peroxidation.