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氧化应激对大鼠心肌梗死后心室重构的影响 被引量:13

Effects of oxidative stress on ventricular remodeling after myocardial infarction in rats
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摘要 目的探讨大鼠急性心肌梗死后氧化应激对心室重构的影响。方法制备雄性SD大鼠急性心肌梗死模型(n=20)和假手术对照(n=12),于手术后6周观察心脏及心脏重量指数(HMI)、左室重量指数(LVMI)、右室重量指数(RVMI)、心功能指标、非梗死区心肌细胞凋亡指数、梗死区及非梗死区心肌胶原含量、Ⅰ型及Ⅲ型胶原比值以及心肌组织的氧化代谢指标。结果心肌梗死后HMI、LVMI、RVMI增加,心功能下降(P<0.05,P<0.01);心肌细胞凋亡指数、非梗死区心肌胶原含量均增加,心肌组织Ⅰ型、Ⅲ型胶原比值升高(P<0.05,P<0.01);心肌组织超氧化物歧化降低,丙二醛含量升高,二者的比值降低(P<0.05);相关性分析提示心肌组织氧化应激水平与心功能指标、心肌细胞凋亡指数、胶原含量、胶原I/III比值均存在相关。结论氧化应激参与心室重构的病理生理过程,干预氧化应激可作为防治心室重构的手段。 Objective To investigate the effects of oxidative stress on ventricular remodeling after acute myocardial infarction (AMI) in rats. Methods AMI was induced in 20 SD rats by ligation of the anterior descending coronary artery, and another 12 rats without the ligation served as the sham-operated group. Six weeks after the operation, the heart mass index (HMI), left ventricular mass index (LVMI), right ventricular mass index (RVMI), the indexes of heart function, cardiac myocyte apoptosis index, collagen content and collagen Ⅰ/Ⅲ ratio and the indexes of oxidative stress were measured. Results After AMI, HMI, LVMI and RVMI increased significantly (P〈0.05), the heart function deteriorated significantly (P〈0.01), and the cardiac myocyte apoptosis index in the non-infarct area, collagen content and collagen Ⅰ/Ⅲ ratio in the infarct and non-infarct areas were all significantly increased (P〈0.05 or 0.01). Myocardial superoxide dismutase (SOD) activity was significantly lowered after AMI, which resulted in significantly increased myocardial malondialdehyde (MDA) level and decreased ratio of SOD/MDA (P〈0.05). Correlations were found between the indexes of oxidative stress in myocardium, those of the heart function and those pertaining to ventricular remodeling after AMI. Conclusion Oxidative stress may be involved in ventricular remodeling after AMI, and antioxidants can be an option for treatment of ventricular remodeling.
出处 《南方医科大学学报》 CAS CSCD 北大核心 2008年第11期2030-2034,共5页 Journal of Southern Medical University
关键词 心肌梗死 心室重构 胶原 细胞凋亡 氧化应激 myocardial infarction ventricular remodeling collagen cell apoptosis oxidative stress
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