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作 者:赵春容[1] 胡文星 岳志杰[3] 张琳[3] 赵雯[1] 左蕾[1] 贺建国[1] 郑宏志[1] 张军[1] 余志斌[3]
机构地区:[1]第四军医大学西京医院超声科 [2]心内科,陕西西安710032 [3]第四军医大学航空航天生理学教研室,陕西西安710032
出 处:《中国医学影像技术》2014年第2期161-166,共6页Chinese Journal of Medical Imaging Technology
基 金:国家自然科学基金(81271580)
摘 要: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 changes of systolic and diastolic function that occurred in left ventricular eardiomyo- cytes during early stage of diabetes rats and the intrinsic links with myocardial ultrastructure and whole cardiac function in rat models. Methods Rats were randomly divided into diabetes mellitus (DM) group and control (CN) group. DM rat models were established through intraperitoneal injection of streptozotocin. Echocardiography, transmission electron micro- scope and video-based edge-detector system were performed respectively at the point of model establishment and 2, 4, 8 weeks later, in order to observe changes of whole cardiac function and myocardial ultrastructure, as well as changes of sys- tolic and diastolic function of cardiomyocytes in left ventricle. Results Compared with CN group, rats in DM group showed larger left ventricular cavity and thinner interventricular septum, and decreased left ventricular ejection fraction in 8 weeks later (all P〈0.05). Rats in DM group appeared myocardial ultrastructure abnormal very mildly 2 Weeks and obvi- ously 4, 8 weeks later. Compared with the same time point of CN group, time from peak to 90% relaxation (TRg0) of rats in DM group slightly prolonged 2 weeks later, while reduction of cell length, peak shortening value (PSi) and maximal velocity of shortening and relengthening (± dL/dt) along with prolongation of time to peak shortening (TPS) and TRg0 occurred 4 and 8 weeks later (all P〈0.05). Conclusion Left ventricular cardiomyocyte of DM rats are damaged in the cel- lular level before whole cardiac malfunction.
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