1-（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

研究1-（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）40min，复灌120min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。

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

To investigate the protective effect of 1-(2 ,6-dimethylphenoxy)-2-(3, 4-dime-thoxyphenylethylamino) 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 perox-idation and the ultramicrostructural changes of myocardial cells were observed. RESULTS: DDPH improved the damage of left ventricular systolic anddiastolicfunction causedbyI/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 peroxi-dation.