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背景:糖尿病心肌病变的结局与糖尿病患者的高心力衰竭发生率密切相关,建立良好的糖尿病心肌病变动物模型为其改善心功能研究极有意义。目的:通过建立2型糖尿病的大鼠及糖尿病心肌病变模型,了解高血糖状况对心肌的影响。设计:以实验动物为研究对象,完全随机分组设计,随机对照研究。单位:一所大学医院内分泌科。方法:实验选用新生雄性Wistar大鼠99只,随机将其分为实验组75只和对照组24只。对照组腹腔注射柠檬酸钠缓冲液,实验组一次性腹腔注射链脲佐菌素90mg/kg,10周后检测糖耐量以确定糖尿病模型的建立;处死后电镜检查其心肌的超微结构。主要观察指标:观察糖尿病大鼠心肌细胞肌原纤维以及线粒体是否改变。结果:实验组空腹血糖犤(8.87±0.76)mmol/L犦轻度高于对照组犤(5.88±0.45)mmol/L犦;实验组餐后2h血糖犤(12.71±0.53)mmol/L犦明显高于对照组犤(6.42±0.4)mmol/L犦,糖耐量异常;电镜下出现肌原纤维呈局灶性变性、肌丝排列紊乱,心肌细胞线粒体肿胀、局灶性增生等改变。结论:该模型是研究2型糖尿病及其心肌病的一种理想载体,为研究其心功能奠定了实验学基础。
BACKGROUND: The outcome of diabetic cardiomyopathy is closely related to the incidence of high heart failure in diabetic patients. It is of great significance to establish a good animal model of diabetic cardiomyopathy for its improvement of cardiac function. Objective: To establish the model of type 2 diabetes mellitus and diabetic cardiomyopathy to understand the effect of hyperglycemia on myocardium. Design: The experimental animals as the research object, completely randomized design, randomized controlled study. Unit: a University Hospital Endocrinology. Methods: Ninety-nine neonatal male Wistar rats were randomly divided into experimental group (n = 75) and control group (n = 24). The control group was intraperitoneally injected with sodium citrate buffer. The experimental group received intraperitoneal injection of streptozotocin (90mg / kg). After 10 weeks, the glucose tolerance was measured to determine the establishment of diabetic model. The ultrastructure of myocardium was observed by electron microscopy after sacrifice. MAIN OUTCOME MEASURES: Myocardial cell myofibrils and mitochondria were observed in diabetic rats. Results: The fasting blood glucose (8.87 ± 0.76) mmol / L 实 in experimental group was slightly higher than that in control group (5.88 ± 0.45) mmol / L 犦; the postprandial blood glucose (12.71 ± 0.53) mmol / L Higher than control group (6.42 ± 0.4) mmol / L 犦, impaired glucose tolerance; under the electron microscope, myofibrils showed focal degeneration, myofilament disordered, mitochondria swelling, focal hyperplasia and other changes. Conclusion: This model is an ideal carrier to study type 2 diabetes mellitus and its cardiomyopathy, which lays the foundation for the study of its cardiac function.