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目的研究链脲佐菌素(STZ)诱导的糖尿病大鼠缺血/再灌注(I/R)心肌的损伤,从心电图、心肌梗死面积、心肌大体和超微结构观察损伤的程度并分析其可能的作用机制。方法采用STZ(45 mg/kg)诱导大鼠糖尿病4周后制备心肌缺血30 min再灌注120 min模型,连续检测心电图变化,用2,3,5-氯化三苯基四氮唑(TTC)染色法测定心肌梗死面积、HE染色和电镜下观察心肌组织结构的改变。结果糖尿病大鼠由I/R损伤引起的心肌梗死面积并没有增加,但是HE染色和电镜下均发现糖尿病心肌损伤更为严重,肌纤维结构消失、心肌细胞膜和细胞核损伤、线粒体降解、血管淤滞、内皮损伤。结论 STZ诱导糖尿病4周的大鼠缺血/再灌注后心肌损伤较非糖尿病大鼠加重。
Objective To investigate the damage of streptozotocin (STZ) -induced myocardial ischemia / reperfusion (I / R) in rats with myocardium injury and to observe the extent of injury from the electrocardiogram, myocardial infarct size, myocardium and ultrastructure and to analyze its possible The mechanism of action. Methods The diabetic rats were induced by STZ (45 mg / kg) for 4 weeks. The model of myocardial ischemia for 30 min followed by 120 min reperfusion was established. The changes of electrocardiogram were detected continuously. The changes of electrocardiogram were observed with 2,3,5-triphenyltetrazolium chloride (TTC ) Staining area, HE staining and electron microscopy changes in myocardial tissue structure. Results The area of myocardial infarction caused by I / R injury did not increase in diabetic rats, but the myocardial injury was more serious in diabetic rats and in HE staining and electron microscopy. The structure of muscle fibers disappeared, myocardial cell membrane and nuclear injury, mitochondrial degradation, vascular stasis, endothelium damage. Conclusion Myocardial injury after STZ-induced diabetic ischemia / reperfusion was more severe in non-diabetic rats than in non-diabetic rats.