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炎症状态下的醛固酮拮抗作用:心肌保护的证据

Aldosterone antagonism in an inflammatory state: evidence for myocardial protection.

作者信息

Ramires Felix J A, Salemi Vera M C, Ianni Barbara M, Fernandes Fábio, Martins Daniel G, Billate Angelina, Neto Edécio Cunha, Mady Charles

机构信息

Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.

出版信息

J Renin Angiotensin Aldosterone Syst. 2006 Sep;7(3):162-7. doi: 10.3317/jraas.2006.026.

DOI:10.3317/jraas.2006.026
PMID:17094053
Abstract

INTRODUCTION

Chagas' disease is one of the most important causes of dilated cardiomyopathy in South and Central America. It is an inflammatory cardiomyopathy. We wanted to investigate whether it could have the same response to aldosterone antagonism as demonstrated before in other dilated cardiomyopathies.

OBJECTIVE

To evaluate the role of spironolactone in myocardial remodelling in a Chagas cardiomyopathy model.

MATERIAL AND METHODS

We studied 60 Sirius Hamsters divided into: control (C) infected (Inf) and Inf plus spironolactone (Infsp, 40 mg/kg/day) groups, for 11 months. Echocardiography with colour doppler was performed. Left ventricular end diastolic diameter (LVEDD), fractional shortening (FS) and corrected isovolumic relaxation time (IRT) were evaluated, as well as interstitial collagen volume fraction (ICVF) and myocardial inflammation.

RESULT

The results demonstrated that survival was improved by use of spironolactone in the chronic phase (p<0.04). Body weight (BW) was C:190 g, Inf:167 g*, Infsp:198 g (p<0.05, compared to C and Infsp), LVEDD/BW was C:0.31, Inf: 0.35, Infsp: 0.29 (p<0.05, compared to C and Infsp), FS was C:38, Inf: 35.5, Infsp: 38 (with no statistical difference) and IRT was C: 23 msec, Inf: 26 msec, Infsp: 22 msec (p<0.05, compared to C and Infsp). ICVF (%) was attenuated at LV (C: 0.34+/-0.1, Inf: 1.75+/-0.7*, Infsp: 0.95+/-0.2*; *p<0.05, p<0.05).

CONCLUSION

Spironolactone attenuated the myocardial remodelling in Chagas cardiomyopathy, reduced mortality during the chronic phase and reduced inflammatory infiltration.

摘要

引言

恰加斯病是南美洲和中美洲扩张型心肌病的最重要病因之一。它是一种炎症性心肌病。我们想研究它是否对醛固酮拮抗剂有与之前在其他扩张型心肌病中所证实的相同反应。

目的

评估螺内酯在恰加斯心肌病模型心肌重塑中的作用。

材料与方法

我们研究了60只Sirius仓鼠,分为:对照组(C)、感染组(Inf)和感染加螺内酯组(Infsp,40毫克/千克/天),为期11个月。进行了彩色多普勒超声心动图检查。评估了左心室舒张末期内径(LVEDD)、缩短分数(FS)和校正等容舒张时间(IRT),以及间质胶原容积分数(ICVF)和心肌炎症。

结果

结果表明,在慢性期使用螺内酯可提高生存率(p<0.04)。体重(BW)分别为:C组190克,Inf组167克*,Infsp组198克(与C组和Infsp组相比,p<0.05);LVEDD/BW分别为:C组0.31,Inf组0.35,Infsp组0.29(与C组和Infsp组相比,p<0.05);FS分别为:C组38,Inf组35.5,Infsp组38(无统计学差异);IRT分别为:C组23毫秒,Inf组26毫秒,Infsp组22毫秒(与C组和Infsp组相比,p<0.05)。左心室ICVF(%)有所减轻(C组:0.34±0.1,Inf组:1.75±0.7*,Infsp组:0.95±0.2*;*p<0.05,p<0.05)。

结论

螺内酯减轻了恰加斯心肌病的心肌重塑,降低了慢性期死亡率,并减少了炎症浸润。

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