Experimental study of improved cardiac remodeling and cardiac dysfunction by Simvastatin

YUAN Qiaoying; et al

doi:10.13406/j.cnki.cyxb.2004.04.028

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Experimental study of improved cardiac remodeling and cardiac dysfunction by Simvastatin

更新时间：2024-01-17

- Experimental study of improved cardiac remodeling and cardiac dysfunction by Simvastatin
- Journal of Chongqing Medical University Issue 4, Pages: 497-499(2004)
- 作者机构：
  
  1. 重庆医科大学临床学院心内科
  2. 重庆医科大学临床学院心内科,重庆,400016
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2004.04.028
  CLC： R542.22
- Published：2004，
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[1]袁侨英,覃数.辛伐他汀改善急性心肌梗死后心室重塑与心功能的实验研究[J].重庆医科大学学报,2004(04):497-499.

YUAN Qiaoying, et al. Experimental study of improved cardiac remodeling and cardiac dysfunction by Simvastatin. [J]. Journal of Chongqing Medical University (4):497-499(2004)
[1]袁侨英,覃数.辛伐他汀改善急性心肌梗死后心室重塑与心功能的实验研究[J].重庆医科大学学报,2004(04):497-499. DOI： 10.13406/j.cnki.cyxb.2004.04.028.

YUAN Qiaoying, et al. Experimental study of improved cardiac remodeling and cardiac dysfunction by Simvastatin. [J]. Journal of Chongqing Medical University (4):497-499(2004) DOI： 10.13406/j.cnki.cyxb.2004.04.028.

摘要

目的 :观察辛伐他汀对急性心肌梗死后大鼠心室重塑及心功能的影响

并探讨其可能的机制。方法 :结扎大鼠冠状动脉前降支造成心肌梗死模型

给予辛伐他汀干预。 8周后

测定心脏重量指数、血流动力学指标、心肌及血液中总—氧化氮合酶（NOS）、诱导型一氧化氮合酶（iNOS）活性

并与假手术组比较。结果 :心肌梗死组大鼠右室重量指数（RVWI）、左室重量指数（LVWI）升高（P <0 .0 1）

外周动脉压（APS）、舒张压（APD）均降低

心率增快（P <0 .0 1）。左室收缩压（LVSP）和心室收缩期室内压上升速率（+dp/dtmax）

心室舒张期室内压下降速率（-dp/dtmax）下降（P <0 .0 1）

左室舒张末压（LVEDP）升高（P<0 .0 1）。血清和心肌NOS、iNOS活性下降（P <0 .0 1）。辛伐他汀干预组较心肌梗死组（M组）RVWI、LVWI下降（P <0 .0 1）

APS、APD、LVSP、+dp/dtmax、-dp/dtmax均回升（P <0 .0 1）

LVEDP回落（P <0 .0 1） ;血清和心肌NOS、iNOS活性升高。结论 :辛伐他汀减轻左室重塑

改善心功能

Abstract

Objective:To investigate the beneficial effects of Simvastatin on cardiac remodeling and cardiac dysfunction after myocardial infarction and its possible mechanisms.Methods:Simvastatin was administered to the rats with myocardial infarction rats by left anterior descending coronary artery ligation.After 8 weeks

cardiac remodeling was observed through right ventricular weight index （RVWI）

and left ventricular weight index （LVWI）.Changes in hemodynamics were observed.The activity of nitric oxide synthase （NOS） and inducible nitric oxide synthase （iNOS） in left ventricle and serum were measured.Results:In the rat model of myocardial infarction RVWI

LVWI increased and activity of NOS and iNOS in ventricle and serum decreased（P

0.01）.Left ventricular systolic pressure（LVSP）

the ventricular pressure rise ratio during systolic period(+dp/dt

max

)

the ventricular pressure rise decay ratio during diastolic period (-dp/dt

max

) decreased（P

0.01） and left ventricular end diastolic pressure （LVEDP） rised（P

0.01）.Simvastatin attenuated RVWI

LVWI （each P

0.01） and NOS iNOS activity increased （P

0.01）.APS APD LVSP +dp/dt

max

-dp/dt

max

rised （P

0.01） and LVEDP decreased （P

0.01）.Conclusion:Simvastatin improves cardiac remodeling and cardiac dysfunction after myocardial infraction.And the improvement of NO availability may be one of the mechanisms.

关键词

辛伐他汀心肌梗死心室重塑一氧化氮

Keywords

simvastatinmyocardial infarctionCardiac remodelingnitric oxide

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