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机构地区:[1]十堰市中西医结合医院内分泌科,湖北十堰442011 [2]湖北医药学院附属东风医院消化内科,湖北十堰442008
出 处:《中国病理生理杂志》2015年第6期988-994,共7页Chinese Journal of Pathophysiology
基 金:湖北省教育厅指导项目(No.B2014054)
摘 要:目的:研究高血压与2型糖尿病联合作用是否能导致小鼠心功能障碍和心肌重塑。方法:将14周龄的2型糖尿病和非糖尿病小鼠经血管紧张素Ⅱ(Ang Ⅱ)给药4周诱导小鼠形成轻度高血压。运用超声波心动描记术和多巴酚丁胺负荷试验评价小鼠左心室功能;HE染色分析左心室心肌细胞的肥大作用;Western blotting测定心肌组织中磷酸化腺苷酸活化蛋白激酶(p-AMPK)的表达水平。结果:与非糖尿病小鼠比较,糖尿病小鼠(DM组)的心脏功能和心肌结构无明显变化;Ang Ⅱ给药不影响2型糖尿病小鼠和非糖尿病小鼠的体重和血糖含量,但血压明显增高;左心室重量和心肌细胞表面积结果分析显示,Ang Ⅱ诱导2型糖尿病小鼠的左心室肥大程度显著大于Ang Ⅱ组;Ang Ⅱ给药的2型糖尿病小鼠左心室的缩短分数和射血分数显著降低,而Ang Ⅱ组小鼠无明显变化;Western blotting结果显示Ang Ⅱ组、DM组和DM+Ang Ⅱ组小鼠左心室组织中p-AMPK的表达量显著降低。结论:2型糖尿病小鼠心脏功能和心肌结构无明显变化,当高血压存在时2型糖尿病小鼠容易发生心脏功能障碍和心肌重塑,提示高血压是2型糖尿病小鼠心脏功能障碍和心肌重塑的关键因子。AIM: To investigate whether the effect of hypertension combined with diabetic can lead to cardiac dysfunction and myocardial remodeling in mice. METHODS: The diabetic mice and non-diabetic mice of 14 weeks old were administered with PBS or angiotensin II (Ang II) for 4 weeks to induce mild hypertension. The left ventricular (LV) function was assessed by echocardiography and dobutamine stress test. The LV tissues were subjected to HE staining to as- sess cardiac hypertrophy. The phospharylated adenosine monophosphate-activated protein kinase (p-AMPK) levels in the LV tissues were determined by Western blotting. RESULTS : Compared with control group, diabetic mice ( DM group) neither displayed marked cardiac dysfunction nor myocardial remodeling. Ang II treatment did not affect body weight and glucose level, but the blood pressure was increased in the diabetic and control mice. Ang II-induced LV hypertrophy in dia- betic mice was significantly higher than that in control mice as assessed by LV masses and cardiomyocyte sizes. Moreover, Ang II-treatment reduced LV fractional shortening and contractility in the diabetic mice, but not in the control mice. The p- AMPK levels were significantly reduced in Ang II group, DM group and DM + Ang II group. CONCLUSION : The cardiac function and cardiac structure of type 2 diabetic mice did not obviously change. Cardiac dysfunction and myocardial remod- eling were easily induced in type 2 diabetic mice when hypertension happened, suggesting that hypertension is a critical fac- tor of cardiac dysfunction and myocardial remodeling in type 2 diabetic mice.
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