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目的探讨心肌胰岛素抵抗对大鼠心肌缺血致心力衰竭的影响。方法雄性Sprague-Dawley(SD)大鼠48只,随机分为对照组(假手术正常心肌)和心力衰竭组,冠状动脉左前降支缝扎术制备大鼠心力衰竭模型。采用超声心动图和心功能分析系统评估大鼠心脏功能。在离体工作心脏灌流模型中,测定葡萄糖和脂肪酸的氧化程度及其在胰岛素刺激下的变化情况。实验结束后取心肌组织观察超微结构并形态学定量测定线粒体损伤程度。结果与对照组比较,心力衰竭组大鼠左心室舒张末期内径增加,而收缩期左心室后壁厚度、心脏射血分数、左心室舒张末期压力、左心室形成压、收缩期和舒张期左心室内压最大变化率明显降低(均P<0.05);胰岛素刺激下,与基础状态下比较,心力衰竭组大鼠葡萄糖氧化量增加率低于对照组[(90±5)%比(229±11)%];脂肪酸氧化量减少率也低于对照组[(47±4)%比(65±3)%,均P<0.05]。心肌细胞超微结构电镜分析显示,心力衰竭组大鼠心肌细胞损伤严重。两组大鼠心肌线粒体损伤程度(Flameng)评分中,心力衰竭组大鼠3、4级心肌线粒体损伤比例显著高于对照组[(76±4)%比(15±7)%,P<0.01]。结论大鼠心力衰竭心肌存在局部的底物氧化水平的胰岛素抵抗,心肌线粒体明显损伤。
Objective To investigate the effect of myocardial insulin resistance on heart failure induced by myocardial ischemia in rats. Methods Forty-eight male Sprague-Dawley (SD) rats were randomly divided into control group (sham operated normal myocardium) and heart failure group, and left anterior descending coronary artery suture was used to prepare rat heart failure model. Cardiac function was assessed using echocardiography and cardiac function analysis system. In isolated working cardiac perfusion models, the degree of oxidation of glucose and fatty acids and their changes under insulin stimulation were determined. After the experiment, the myocardial tissue was taken to observe the ultrastructure and quantitatively determine the degree of mitochondrial damage. Results Compared with the control group, left ventricular end-diastolic diameter of heart failure rats increased, while systolic left ventricular posterior wall thickness, cardiac ejection fraction, left ventricular end-diastolic pressure, left ventricular pressure, systolic and diastolic left ventricular The maximum rate of change of glucose in heart failure group was significantly lower than that in control group [(90 ± 5)% vs (229 ± 11), P <0.05] )%]. The reduction rate of fatty acid oxidation was also lower than that of the control group [(47 ± 4)% vs (65 ± 3)%, both P <0.05]. Myocardial ultrastructure Electron microscopy analysis showed that heart failure rat myocardial cells were severely damaged. In Flameng scores of myocardial mitochondria in both groups, the percentage of myocardial mitochondrial damage in rats with heart failure group was significantly higher than that in control group (76 ± 4)% (15 ± 7)%, P <0.01 ]. Conclusion There is a local oxidation of insulin in myocardium of rats with heart failure, and myocardial mitochondria are obviously damaged.