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高盐饮食对大鼠心肌组织的影响及相关机制探讨
引用本文:李静宜,张少玲,严励,任萌,王川,程桦.高盐饮食对大鼠心肌组织的影响及相关机制探讨[J].中华医学杂志,2009,89(22).
作者姓名:李静宜  张少玲  严励  任萌  王川  程桦
作者单位:中山大学附属第二医院内分泌科,广州,510120
摘    要:目的 观察高盐饮食对大鼠血压和左心室心肌的影响,并探讨其有关机制.方法 采用1%氯化钠溶液喂养SD大鼠8周,建立高盐饮食大鼠模型,并设正常对照组.用tail-cuff法监测高盐组和正常组血压变化、超声检查左心室结构变化、电子显微镜观察心肌超微结构、测定血钠、血氯浓度和24 h尿钠、尿氯排出量、检测左心室心肌组织还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶p22phox亚基和p47phox亚基mRNA及蛋白表达水平,并检测NADPH氧化酶活性和血清8-异前列烷浓度.结果 正常组(125±3)mm Hg,高盐组血压无显著变化(128±4)mm Hg,P0.05],但左心室质量指数(2.28±0.15)mg/g比正常组增加(2.06±0.10)mg/g,P<0.05],心脏超声检查可见左心室前、后壁厚度均比正常组增加(2.29±0.21)mm比(1.90±0.25)mm,P<0.05;(2.22±0.17)mm比(1.99±0.16)mm,P<0.05],心脏舒张功能降低.心肌组织NADPH氧化酶的亚基p22phox、p47phox mRNA和蛋白表达水平均增加,NADPH氧化酶活性增强(0.142±0.023) μmol·min-1·mg-1比(0.332±0.015)μmol·min-1·mg-1,P<0.05],血清8-异前列烷浓度(1117±86)pg/ml比正常对照增加(327±80)pg/ml,(P<0.05).结论 高盐饮食可在不影响血压的情况下,导致左心室心肌组织氧化应激反应增强、左心室肥大、心脏舒张功能降低.

关 键 词:  血压  左心室肥大  氧化应激

Primary study on the effects of high-salt diet on the myocardium and the related mechanisms
LI Jing-yi,ZHANG Shao-ling,YAN Li,REN Meng,WANG Chuan,CHENG Hua.Primary study on the effects of high-salt diet on the myocardium and the related mechanisms[J].National Medical Journal of China,2009,89(22).
Authors:LI Jing-yi  ZHANG Shao-ling  YAN Li  REN Meng  WANG Chuan  CHENG Hua
Abstract:Objective The study was to evaluate the effects of high-salt diet on the blood pressure and myocardium in Sprague-Dawley rats and to investigate the related mechanisms. Methods Rat model of high-salt diet was established by receiving standard rat chow with salt concentration of 0.3% and additional salt load via the drinking water (1% sodium chloride solution). Systolic blood pressure was measured by The indirect tail-cuff method in the rots on high-salt and normal-salt diet. The rats were placed in metabolic cages. Food intake and urine volume were recorded. The sodium and chloride in plasma and urine were measured. Transthoracic echecardiographic studies were performed at the eighth week with an echocardiographic system. The pathological variations of the myocardium were observed by the electron microscopy. The p22phox and p47phox mRNA expressions were analyzed by real time RT-PCR. The p22phox and p47phox protein expressions were analyzed by Western blot. The NADPH oxidase activity of myocardium and the serum 8-isoprostane levels were measured. Results Left ventricular hypertrophy (all P<0.05) and the decreased diastolic function of left ventricle without significantly elevated blood pressure (128±4)mm Hg versus (125±3)mm Hg in controls, P0.05] were found in the rats on high-salt diet, compared to those in the rats on normal-salt diet. Furthermore, mRNA and protein expressions of the p22phox and p47phox, and the NADPH oxidase activity of myocardium were increased (0.332±0.015) isoprostane levels (1117±86) pg/ml versus (327±80) pg/ml in controls, P<0.05] were also significantly increased in the rats on high-salt diet. Condusion High-salt diet might lead to left ventricular hypertrophy and the decreased diastolic function of left ventricle through oxidative stress without significantly elevated blood pressure.
Keywords:Salt  Blood pressure  Left ventricular hypertrophy  Oxidative stress
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