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作 者:汪俊元[1] 王安才[1] 曹蘅[1] 何世宝[1] 汪念东[1] 吴明[1]
机构地区:[1]皖南医学院弋矶山医院心血管内科,241001
出 处:《疑难病杂志》2012年第11期857-859,F0003,共4页Chinese Journal of Difficult and Complicated Cases
基 金:皖南医学院中青年科研基金项目(No.WK200710F)
摘 要:目的观察血管紧张素(1-7)[Ang-(1-7)]对压力负荷增高所致大鼠心肌重构的影响。方法 30只雄性SD大鼠随机分为3组:假手术组、腹主动脉缩窄(AAC)组和Ang-(1-7)组。后2组采用腹主动脉缩窄术建立心脏压力负荷增高动物模型。术后1 d开始,Ang-(1-7)组大鼠经渗透性微量泵持续颈静脉输注Ang(1-7)25μg·kg^(-1)·h^(-1),假手术组及AAC组经渗透性微量泵给予等量生理盐水。4周后鼠尾容积法测量收缩压;称取左心室质量(LVM),计算左心室质量指数(LVMI);HE染色检测心肌细胞平均直径;放免法测定血浆和心肌血管紧张素Ⅱ(AngⅡ)浓度。结果与假手术组相比,AAC组、Ang-(1-7)组收缩压、LVM、LVMI、心肌AngⅡ浓度、心肌细胞平均直径均显著升高(P<0.05,P<0.01)。与AAC组相比,Ang-(1-7)组血压和心肌AngⅡ浓度差异无统计学意义(P>0.05),但LVM、LVMI、心肌细胞平均直径明显降低(均P<0.05)。结论 Ang-(1-7)可改善腹主动脉缩窄高血压大鼠左室肥厚,逆转心肌重构。Objective To investigate the effect of angiotensin (1-7) on myocardial remodeling which induced by pres- sure overload in rats. Methods Thirty SD rat were randomly divided into 3 groups. Left ventricular hypertrophy was induced by abdominal aortic constriction (AAC) and received angiotensin ( 1-7 ) (25 μg·kg-1·h-1) ( n = 10). Sham operated rats ( n = 10) and untreated AAC rats ( n = 10) served as controls. Systolic blood pressure (SBP) and LVMI were determined, cardiomyocytes diameter were measured by HE stain; plasma angiotensin II and myocardial angiotensin II levels was detected by radioimmunoassay. Results Compared With sham operation group,SBP, LVMI, mean diameter of cardiomyocytes and myo- cardial angiotensin II concentration in AAC rats were significantly increased ( P 〈 0.05, P 〈 0.01 ). SBP and myocardial an- giotensin II concentration had no significant differences between AAC rats and Ang (1-7) rats ( P 〉 0.05 ), While LVMI, mean diameter of cardiomyocytes in Ang ( 1-7 ) rats were Significantly decreased ( all P 〈 0.05 ). Conclusion Ang ( 1-7 ) could prevent the development of myocardial hypertrophy in pressure overloaded rats and reverse myocardial remodeling.
关 键 词:血管紧张素(1-7) 高血压 左室肥厚 心肌重构 大鼠
分 类 号:R544.1[医药卫生—心血管疾病]
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