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【目的】在建立链脲佐菌素(STZ)诱导糖尿病小鼠心肌梗死模型的基础上,进行心脏梗死区和梗死周边区指标分析,探讨糖尿病合并心肌梗死的病理过程。【方法】选用C57/B6雄性小鼠,采用腹腔注射STZ(剂量为45mg·kg-1·d-1)法复制糖尿病模型,并在糖尿病模型造模成功第7周实施心肌梗死手术,结扎冠状动脉左前降支复制STZ诱导糖尿病合并心肌梗死模型。在术后检测心脏梗死区和梗死周边区指标改变,探讨糖尿病心肌梗死小鼠的病理过程。【结果】与心肌梗死组比较,在术后第4天,糖尿病心肌梗死组梗死周边区细胞凋亡显著增加(P<0.01);第21天,糖尿病心肌梗死组的梗死周边区毛细血管密度显著减少(P<0.01),梗死纤维化比例显著增加(P<0.01);第49天,糖尿病心肌梗死组梗死面积显著增加(P<0.01)。在术后第4天,糖尿病心肌梗死组梗死周边区氧化应激显著增加(P<0.05)。【结论】对STZ诱导糖尿病合并心肌梗死模型小鼠进行心脏梗死区和梗死周边区指标分析,可为深入研究临床上糖尿病合并心肌梗死并发症的病理生理机制和治疗方案提供模型基础。
【Objective】 On the basis of STZ-induced myocardial infarction model in diabetic mice, the aim of this study was to analyze the indexes of myocardial infarction and infarct peripheral areas to explore the pathological process of diabetes complicated with myocardial infarction. 【Methods】 C57 / B6 male mice were used to replicate the diabetic model by intraperitoneal injection of STZ (45mg · kg-1 · d-1), and myocardial infarction was performed in the seventh week after model establishment in diabetic model. Artery left anterior descending branch replicates STZ - induced diabetic mellitus with myocardial infarction. After myocardial infarction in the detection of infarct and peripheral areas index changes, explore the pathological process of diabetic mice with myocardial infarction. 【Results】 Compared with myocardial infarction group, on the 4th day after operation, the apoptosis in infarcted peripheral area was significantly increased in diabetic myocardial infarction group (P <0.01). On the 21st day, the capillary density in infarcted peripheral area was significantly higher in diabetic myocardial infarction group (P <0.01), and the proportion of infarcted fibrosis increased significantly (P <0.01). On the 49th day, infarct size in diabetic myocardial infarction group increased significantly (P <0.01). On the fourth postoperative day, the oxidative stress in infarcted area was significantly increased in diabetic myocardial infarction group (P <0.05). 【Conclusion】 The analysis of cardiac infarction area and infarct peripheral area in diabetic mice with STZ-induced myocardial infarction may provide a model basis for further study on the pathophysiological mechanism and treatment of diabetic complications associated with myocardial infarction.