论文部分内容阅读
目的探讨糖尿病大鼠早期病变过程中左心室心肌细胞收缩、舒张功能的变化及其与细胞超微结构、整体心脏功能变化之间的内在联系。方法向大鼠腹腔注射链脲佐菌素建立糖尿病模型(DM组),并设立对照组(CN组)。应用超声心动图、透射电镜和可视化动缘探测系统观测两组大鼠成模起始点、2周、4周及8周时左心室整体功能和超微结构变化以及心肌细胞收缩、舒张功能改变。结果 8周时DM组较CN组左心室心腔扩大、室间隔变薄、射血分数降低(P均<0.05)。2周时DM组心肌超微结构出现轻度异常,4周和8周时DM组心肌超微结构出现明显病变。与同时间点CN组比,2周时DM组大鼠心肌细胞舒张90%时程(TR90)轻度延长(P<0.05),4周和8周时心肌细胞长度缩短,收缩幅值(PS%)与最大缩短、复长速率(±dL/dt)减低,收缩达峰时程(TPS)及TR90延长(P均<0.05)。结论糖尿病大鼠心肌在整体功能出现异常前已发生不可逆的细胞水平损伤。
Objective To investigate the changes of left ventricular myocytes contractile and diastolic function and their relationship with the changes of ultrastructure and cardiac function in diabetic rats. Methods The diabetic model was established by intraperitoneal injection of streptozotocin (DM group), and the control group (CN group) was established. Echocardiography, transmission electron microscopy and visualization of the dynamic detection system were used to observe the onset of modeling at 2, 4, and 8 weeks in left ventricular function and ultrastructure changes and myocardial cell contraction, diastolic function changes. Results In the DM group, the left ventricular cavity was enlarged and the ventricular septum was thinner and the ejection fraction was lower at 8 weeks (all P <0.05). At 2 weeks, the myocardial ultrastructure of DM group showed mild abnormality. At 4 weeks and 8 weeks, myocardial ultrastructure of DM group showed obvious pathological changes. Compared with CN group at the same time point, the myocardial cell length (TR90) was slightly prolonged (P <0.05) at 2 weeks in DM group and the length of myocardial cells was shortened at 4 and 8 weeks %), Maximal shortening and long-term growth rate (± dL / dt), systolic peak duration (TPS) and TR90 prolongation (all P <0.05). Conclusion The irreversible damage to the myocardium of diabetic rats occurs before the abnormal function.