我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

醛固酮诱导的心肌重构及非洛地平的干预作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第2期
页码:
186
栏目:
基础研究
出版日期:
2009-03-30

文章信息/Info

Title:
Felodipine attenuates myocardial remodeling induced by aldosterone
作者:
孙建琦马礼坤余华冯克福
安徽医科大学附属安徽省立医院心血管内科,安徽 合肥 230001
Author(s):
SUN Jian-qi MA Li-kun Yu Hua Feng Ke-fu
Department of Cardioangiology, Anhui Provincial Hospital, Anhui Medical University, Hefei 230001, Anhui, China
关键词:
非洛地平醛固酮心肌重构
Keywords:
felodipinealdosteronemyocardial remodeling
分类号:
R972.4
DOI:
-
文献标识码:
A
摘要:
目的 研究非洛地平(felodipine,Fel)在醛固酮(aldosterone,Ald)诱导的心肌重构中的保护作用及其可能的机制。方法 SD大鼠32只随机分为4组(每组n=8),即对照组、Ald组、Ald+Fel组和Ald+螺内酯(spironolactone,Spi)组。Ald组:以Ald 18 μg/d皮下注射,连续4周;对照组:注射等量生理盐水4周;Ald+Fel组:以Ald 18 μg/d皮下注射,同时给于Fel 5 mg/(kg·d)灌胃,连续4周;Ald+Spi组:以Ald 18 μg/d皮下注射, 同时给予Spi 20 mg/(kg·d)灌胃,连续4周。比较各组大鼠的左心室质量(LVW)及全心质量(HW)与体质量(BW)的比值,心肌组织匀浆超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,心肌胶原面积(CA),以及心肌细胞凋亡指数(AI)。结果 与Ald组相比, 对照组、Ald+Fel组和Ald+Spi组大鼠的LVW/BW,HW/BW,CA和AI均减少,对照组和Ald+Spi组大鼠MDA的含量较Ald组减少,SOD的含量较Ald组增加(P<0.01);Ald+Fel组大鼠SOD和MDA的含量与Ald组相比无明显差异。结论 Fel能够改善Ald诱导的心肌肥大和心肌细胞凋亡,但不能改善Ald诱导的氧化应激水平的增加。
Abstract:
AIM To investigated the protective effects of felodipine(Fel) in aldosterone (Ald) induced myocardial remodeling. METHONDS Thirty-two rats were randomly assigned into 4 groups, 8 rats in each group: namely, Control group, Ald group Ald 18 μg/d hypodermic injection for 4 weeks), Ald+Fel group [Ald 18 μg/d hypodermic injection and Fel 5 mg/(kg·d) intragastric administration for 4 weeks], and Ald+Spi group (Ald 18 μg/d hypodermic injection and Spi 20 mg/(kg·d) intragastric administration for 4 weeks). All the animals were sacrificed after 4 weeks and the ratio of left ventricular weight/body weight (LVW/BW) and heart weight/body weight (HW/BW), the concentration of SOD and MDA in cardiomyocyte homogenate, collagen area (CA) and apoptosis index (AI) were analyzed. RESUSTS Compared with those in Ald group, LVW/BW, HW/BW, CA and AI were lower in control group, Ald+Fel group and Ald+Spi group. SOD was higher and MDA was lower in control group and Ald+Spi group (P<0.01), but not in Ald+Fel group. CONCLUSION Felodipine can improve aldosterone-induced myocardial hypertrophy and cardiomyocyte apoptosis but not aldosterone-induced oxidative stress.

参考文献/References

[1] 杨永健,速晓华,李刚,等. 钙通道阻滞剂对心肌重构保护机制的研究[J]. 中国药理学通报, 2005, 21(3):310-313.

[2] 欧阳迎春,罗兴林. 非洛地平与苯那普利对高血压病患者心肌纤维化及左室肥大逆转作用的对比研究[J]. 临床荟萃, 2001, 16(24):1126-1127.

[3] Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction[J]. N Engl J Med, 2003, 348(14):1309-1321.

[4] Kotlyar E, Vita JA, Winter MR, et al. The relationship between aldosterone, oxidative stress, and inflammation in chronic, stable human heart failure[J]. J Card Fail, 2006, 12(2):122-127.

[5] 龙元,曾秋棠. 醛固酮对新生大鼠心肌细胞凋亡的影响[J]. 华中科技大学学报(医学版), 2006, 35(6):737-739.

[6] Bénitah JP, Vassort G. Aldosterone upregulates Ca2+ current in adult rat cardiomyocytes[J]. Circ Res, 1999, 85(12):1139-1145.

[7] Romain P, Sylvain R, Yannis SM, et al. A direct relationship between plasma aldosterone and cardiac L-type Ca2+ current in mice[J]. J Physiol, 2005, 569(1):153-162.

[8] 杨大春,张 鑫 ,杨永健,等.醛固酮诱导心肌成纤维细胞增殖的信号转导[J]. 心脏杂志, 2007, 19(3):269-271.

[9] Liao X, Liu JM, Du L, et al. Nitric oxide signaling in stretch-induced apoptosis of neonatal rat cardiomyocytes[J]. FASEB J, 2006, 20(11):1883-1885.

[10]Ahokas RA, Warrington KJ, Gerling IC, et al. Aldosteronism and peripheral blood mononuclear cell activation: a neuroendocrine-immune interface[J]. Circ Res, 2003, 93(10):e124-e135.

备注/Memo

备注/Memo:
收稿日期:2008-7-21.基金项目:安徽省优秀青年基金项目资助(04043054) 通讯作者:马礼坤,主任医师,教授,博士,主要从事冠心病介入治疗的研究Email:Malk2002cn@yahoo.com.cn 作者简介:孙建琦,硕士生Email:jianqisun@163.com
更新日期/Last Update: 2009-04-16