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机构地区:[1]广西中医学院第一附属医院急诊ICU,广西南宁530023 [2]广西医科大学第一附属医院心内科,广西南宁530023
出 处:《心血管康复医学杂志》2009年第1期57-60,共4页Chinese Journal of Cardiovascular Rehabilitation Medicine
摘 要:目的:探讨普伐他汀对高蔗糖饲料喂养诱导的胰岛素抵抗Wistar大鼠左室重量的影响及其可能机制。方法:雄性Wistar大鼠被分成3组:(1)胰岛素抵抗组(IR组,10只):高蔗糖饲料喂养12周;(2)普伐他汀组(P组,10只):高蔗糖饲料喂养12周,后4周每只每天加普伐他汀5 mg/kg灌喂;(3)正常对照组(5只):普通饲料喂养12周。12周后量血压、断尾留取血标本检测血糖、血脂、血清胰岛素水平;处死动物,留取心肌标本检测左室相对重量(LVRW)、心肌内皮素(ET)和血管紧张素Ⅱ(AngⅡ)水平。结果:与对照组比较,IR组大鼠LVRW、心肌ET和AngⅡ水平明显升高,而胰岛素敏感指数(ISI)则明显降低(P均<0.01);体重和血压差异没有显著性(P>0.05)。普伐他汀干预后的Wistar大鼠除了血压、心肌AngⅡ水平无显著差异外,心肌ET水平,LVRW均较IR组明显减少,胰岛素敏感指数(ISI)则明显回升(P<0.01)。结论:普伐他汀可改善胰岛素抵抗Wistar大鼠的左室肥厚,其机制可能与改善胰岛素抵抗及减少局部心肌ET水平有关。Objective: To investigate the effect of pravastatin on left ventricular mass of rats with insulin resistance in- duced by high-sucrose chow. Methods: Weight-matched male Wistar rats were randomly divided into three groups (10 rats in each group). A high-sucrose chow was given in insulin resistance group and the ordinary chow given in control group for 12 weeks. After the models of insulin resistance induced Successfully. the rats of pravastatin group received a dose of 5 mg/kg·d of pravastatin for 4 weeks. Then the concentrations of endothelin (ET) and angiotensin Ⅱ (Ang Ⅱ ) in myocardial tissue sample were also assayed in each group. Blood pressure, blood glucose and insulin sensitivity index (ISI) were determined. The left ventricular relative weight (LVRW) was calculated by the following formula: the weight of left ventricle+the weight of septum/body weight for heart of kill rat. Results: The concentration of ET and Ang II in myocardial tissue sample, and the LVRW in insulin resistance group than those in control group (P〈0. 01 all), however, the ISI was significantly lower in insulin resistance group (P〈0.01). As compared with insulin resistance group, the concentration of ET in myocardial tissue sample, and LVRW were significantly lower in pravasta-tin group (P〈0.01). Conclusion: Pravastatin can ameliorate myocardial hypertrophy of rats with insulin resistance by improving the insulin resistance, inhibiting the release of ET in myocardium tissue.
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