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|本期目录/Table of Contents|

卡维地洛对心梗大鼠远期心室重构的影响及其作用机制

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2014年第4期
页码:
411-415
栏目:
基础研究
出版日期:
2014-04-25

文章信息/Info

Title:
The effect and mechanism of carvedilol long-time ventricular remodeling in rats with myocardial infarction
作者:
梁羡方1; 赵新军2; 谢绍洽1; 陈彩仙1
(1.广东省阳东县人民医院心内科，广东 阳江 529931；
2.南方医科大学中医药学院心内科，广东 广州 510515)
Author(s):
LIANG Xian-fang1;  ZHAO Xin-jun2;  XIE Shao-qia1;  CHEN Cai-xian1
(1.Department of Cardiology, People’s Hospital, Yangdong County, Yangdong 529900, Guangdong, China;
2.Department of Cardiology, Hospital of Integrated Traditional Chinese and Western Medicine, Southern Medical University, Guangzhou 510515, Guangdong, China)
关键词:
卡维地洛; 心肌梗死; 远期心室重构; 大鼠
Keywords:
carvedilol;  myocardial infarction;  long-time ventricular remodeling;  rats
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的:探讨卡维地洛(Carv)对心肌梗死(MI)大鼠心室心肌重构的影响及其作用机制。方法： 结扎30只大鼠左冠状动脉建立MI模型后，随机分为Carv组(n=15)及MI组(n=15)。再另设假手术(Sham)组(n=15)。Carv组给予Carv(日剂量2 mg/kg)，分2次灌胃；Sham组及MI组均给予等量蒸馏水灌胃。24周后，观察心室重构和左室非梗死区心肌内4-羟基 壬烯醛（4-HNE）和过氧化物丙二醛（MDA）的含量及表达。结果： 24周后， 超声显示，与Sham组比较，MI组大鼠心功能明显降低,左室舒张末期内径（LVEDD）明显增大，左室短轴缩短率（FS）和心脏射血分数（EF）明显降低(P<0.05，P<0.01)。MI组大鼠左室非梗死区心肌内4-HNE和MDA的含量明显增加，表达明显增强（P<0.05，P<0.01）。Carv组大鼠左室非梗死区心肌组内4-HNE和MDA的含量比MI组明显降低（P<0.05，P<0.01）。结论： MI 6月后，心肌内4-HNE、MDA的活性仍然较高，氧化应激反应仍持续，Carv可以促进活性醛的代谢，对心脏具有保护作用，可改善预后。
Abstract:
AIM:To explore the effect and protective mechanism of carvedilol in long-time ventricular remodeling in rats with myocardial infarction (MI). METHODS: Rat models with MI were established by the ligation of left anterior descending coronary artery. Rats with myocardial infarction were randomly divided into carvedilol group (Carv, 15), myocardial infarction group (MI, 15) and sham-operated group (Sham, 15). Animals in carvedilol group were treated with carvedilol ［2 mg/(kg·day)］ by gastric gavage and animals in the other two groups were given the same amount of distilled water. After 24 weeks of treatment, the extent of ventricular remodeling and the expression of 4-HNE and MDA were measured in the noninfarcted myocardium. RESULTS: Twenty-four weeks after MI, LVEDD in the MI group significant increased compared with that in the sham group (P<0.05). EF and FS values significant decreased compared with those in the Sham group and the Carv group (P<0.01). Expression of 4-HNE and MDA in the MI group significantly increased (P<0.05, P<0.01). Expression of 4-HNE and MDA in the Carv group decreased compared with that in the MI group (P<0.05, P<0.01). CONCLUSION: Six months after myocardial infarction, the expression of 4-HNE and MDA in noninfarcted myocardium is still active and the oxidative stress reaction is still sustained. Carvedilol can promote the metabolism of active aldehyde, protect the heart and improve the prognosis after MI.

参考文献/References

[1]Siems W,Grune T.Intracellular metabolism of 4-hydroxynonenal[J].Mol Aspects Med,2003,24(4/5):167-175.
[2]Alary J,Guéraud F,Cravedi JP.Fate of 4-hydroxynonenal in vivo:disposition and metabolic pathways[J].Mol Aspects Med,2003,24(4/5):177-187.
[3]Ma H,Guo R,Yu L,et al.Aldehyde dehydrogenase 2(ALDH2)rescues myocardial ischaemia/reperfusion injury: role of autophagy paradox and toxic aldehyde[J].Eur Heart J,2011,32(8):1025-1038.
[4]Gong D,Zhang Y,Zhang H,et al.Aldehyde dehydrogenase-2 activation during cardioplegic arrest enhances the cardioprotection against myocardial ischemia-reperfusion injury[J].Cardiovasc Toxicol,2012,12(4):350-358.
[5]Dolinsky VW,Chan AY,Robillard Frayne I,et al.Resveratrol prevents the prohypertrophic effects of oxidative stress on LKB1[J].Circulation,2009,119(12):1643-1652.
[6]Chaudhary P,Sharma R,Sharma A,et al.Mechanisms of 4-hydroxy-2-nonenal induced pro- and anti-apoptotic signaling[J].Biochemistry,2010,49(29):6263-6275.
[7]Raza H,John A.4-hydroxynonenal induces mitochondrial oxidative stress, apoptosis and expression of glutathione S-transferase A4-4 and cytochrome P450 2E1 in PC12 cells[J].Toxicol Appl Pharmacol,2006,216(2):309-318.
[8]Soh Y,Jeong KS,Lee IJ,et al.Selective activation of the c-Jun N-terminal protein kinase pathway during 4-hydroxynonenal-induced apoptosis of PC12 cells[J].Mol Pharmacol,2000,58(3): 535-541.
[9]张润峰,王继生.建立大鼠心肌梗死模型的若干问题探讨[J].山西医科大学学报,2004,35(1):13-15.
[10]刘开宇,田 海,孙 露,等.标准化大鼠心肌梗死模型的制作[J].哈尔滨医科大学学报,2007,41(6):531-534.
[11]王 勇，高大中，殷跃辉，等.大鼠心肌梗死模型建立方法选择及心电图表现[J].中国实验动物学报,2011,19(6):525-529.
[12]吴 强,李隆贵,蔡运昌,等.不同剂量卡维地洛对心衰大鼠心肌氧化应激和细胞凋亡的影响[J].心脏杂志,2003,15(5):410-413.
[13]孙梅芹,闫 翔,王 建,等. 不同肾上腺素能受体阻滞剂对超压力负荷大鼠左室重构的影响[J].心脏杂志,2008,20(5):537-540.
[14]李 保,马业新,解 军,等.卡维地洛改善心梗大鼠心肌氧化应激状态[J].中国药理学通报,2005,21(6):751-754.

备注/Memo

备注/Memo:
收稿日期：2013-10-11.作者简介：梁羡方，主治医师 Email：Liangxf980@163.com 共同第一作者：赵新军，博士生 Email：zxjhwxm@sina.com
更新日期/Last Update: 2014-05-06