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作 者:许闽广[1] 董战玲[1] 翁启芳[1] 周升[2] 吉丽敏[3] 符史干[1]
机构地区:[1]海南医学院生理学教研室,海南海口571101 [2]海南医学院化学分析实验室,海南海口571101 [3]海南医学院机能实验室,海南海口571101
出 处:《海南医学院学报》2006年第2期109-111,共3页Journal of Hainan Medical University
基 金:国家自然科学基金资助课题(NO.30260032)
摘 要:目的:建立容量超负荷大鼠模型,测量全心室重/体重(WVW/BW)、左心室重/体重比值(LVW/ BW)和血浆血管紧张素Ⅱ水平、血浆肾素活性,观察容量超负荷条件下大鼠心肌肥大与血管紧张素Ⅱ、肾素之间的关系,探讨容量超负荷引起心肌肥大的机制。方法:穿刺A-V联合壁造瘘制造大鼠容量超负荷模型。结果:手术组(0.6±0.1)与正常对照组(0.4±0.1)及假手术组(0.4±0.1)比较,LVW/ BW有显著性差异(P<0.05);手术组(2.1±0.2)与正常对照组(1.8±0.2)及假手术组(2.0±0.2)比较, LVW/BW无显著性差异(P>0.05)。手术组(3 665.0±1 637.4)与正常对照组(1 900.0±1 300.0)及假手术组(1905.3±1302.4)比较,血管紧张素Ⅱ有显著性差异(P<0.05)。手术组(87.3±47.1)与正常对照组(170.0±70.0)及假手术组(172.1±76.3)比较,血浆肾素活性有显著性差异(P<0.05)。结论:容量超负荷可引起大鼠心肌肥大,引起肥大的机制可能与心肌细胞对容量超负荷的机械刺激信号产生应答反应,引起心肌细胞跨膜转导信号改变有关,其中血管紧张素Ⅱ具有特别重要的作用。在容量超负荷下血管紧张素Ⅱ的升高是否存在其他不依赖肾素的途径尚需要进一步的研究。Objective: To investigate the mechanism of myocardial hypertrophy resulted from volume overload by means of testing the indexes of HW/BW, LVW/BM and the changes of plasma AngII level and plasma rennin activity (PRA) in the rats with myocardial hypertrophy by volume overload. Methods: Abdominal aorta-inferior vena cava fistula was performed on the rats of volume overload group (operative group), compared with the sham operative group and the control group. The indexes of HW/BW, LVW/BM were measured in each group after 60 days. At the same time, the plasma AngⅡ level and PRA were observed. Results: The indexes of HW/BW, LVW/BM of the operative group were significantly increased compared with the control group and the sham operated group. There were significant differences of the plasma level of AngⅡ and PRA among the three groups. Conclusion: These results suggest that volume overload can cause the hypertrophy of cardiomyocytes and the mechanisms of myocardial hypertrophy by volume overload might be cardiomyocyte response to mechanical stimuli by volume overload and AngⅡ system.
分 类 号:R542.2[医药卫生—心血管疾病]
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