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|

卡维地洛和喹那普利初始用药次序对心衰大鼠 心功能及血清MCP-1的影响

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第5期
页码:
634-638
栏目:
基础研究
出版日期:
2009-07-14

文章信息/Info

Title:
Effect of combined sequences between carvedilol and quinapril on serum MCP-1 and heart function in rats with heart failure
作者:
彭彬12蒋学俊1李晓艳1
1.武汉大学人民医院心内科,湖北 武汉 430060;2.郴州市第一人民医院心内科,湖南 郴州 423000
Author(s):
PENG Bin12 JIANG Xue-jun1 LI Xiao-yan1
1.Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan 430060, Hubei, China; 2.Department of Cardiology, First Peoples Hospital of Chenzhou, Chenzhou 423000, Hunan, China
关键词:
心力衰竭单核趋化蛋白-1心功能卡维地洛喹那普利大鼠
Keywords:
heart failure monocyte chemoattractant protein-1 heart function carvedilol quinapril rat
分类号:
R541.6
DOI:
-
文献标识码:
A
摘要:
目的: 比较不同次序的卡维地洛和喹那普利联合给药对心衰大鼠心功能及血清单核趋化蛋白-1(MCP-1)水平的影响;明确心衰大鼠心功能的变化与MCP-1水平改变的关联。方法: 复制阿霉素心肌病-心衰模型,以ELISA法检测大鼠血清MCP-1的水平;用超声心动图评估心功能。以不同次序的药物干预16周后,比较其对心衰大鼠血清MCP-1的水平及心功能的影响,并对两者之间的变化进行相关性分析。结果: 实验组(心衰组)大鼠血清MCP-1的水平显著升高,且随着心衰程度的加剧而升高。用卡维地洛和喹那普利干预后,大鼠血清MCP-1的水平下调,心功能明显改善;不同次序的给药方案对大鼠的存活率、血清MCP-1的水平和心功能的影响无显著差异。心衰大鼠心功能的改善与血清MCP-1水平的下调呈正相关(rA=0.61,rB=0.64;P≤0.01)。结论: 血清MCP-1的水平是反映大鼠心衰程度的客观指标。卡维地洛与喹那普利能显著改善大鼠的心功能并下调血清MCP-1的水平。不同次序的用药方案对改善心功能与下调血清MCP-1水平同样有效、安全。
Abstract:
AIM: To compare the effect of combined sequences between carvedilol and quinapril on serum MCP-1 level and heart function in rats with heart failure and to identify the relation between the change of serum MCP-1 levels and the alteration of heart function. METHODS: The model of ADR-DCM/CHF was reproduced, serum levels of MCP-1 was determined by means of enzyme-linked immunosorbent assay (ELISA) and heart function was evaluated with ultrasonic cardiography. Changes in serum MCP-1 and heart function after combined drug intervention between carvedilol and quinapril for 16 weeks were compared with those in control group. Correlations between the change of serum MCP-1 and the alteration of heart function were analyzed. RESULTS: Compared with those in control group, serum MCP-1 levels of rats with heart failure were higher and serum levels of MCP-1 increased with the aggravation of the heart function. Serum MCP-1 was downregulated and heart function was improved after drug intervention with carvedilol and quinapril. Dose schedule with different sequences had no marked effect on survival rates, serum MCP-1 and heart function in rats. There were positive correlations between the amelioration of heart function and the downregulation of serum MCP-1 in rats with heart failure (rA=0.61, rB=0.64; P≤0.01). CONCLUSION: The level of serum MCP-1 is an objective index for estimating the degree of heart failure. Both carvedilol and quinapril improve heart function in rats with heart failure by decreasing the level of serum MCP-1. The sequence of using carvedilol and quinapril makes no marked difference in the downregulation of the serum MCP-1 in rats with heart failure and amelioration of heart function.

参考文献/References

[1] Siveski-Iliskovic N, Hill M, Chow DA, et al. Probucol protects against adriamycin cardiomyopathy without interfering with Antitumor effect[J]. Circulation, 1995, 91(1):10-15.

[2] Singal PK, Iliskovic N. Doxorubicin induced cardiomyopathy[J]. N Engl J Med, 1998, 339(13):900-905.

[3] Lisman KA, Stetson SJ, Koerner MM, et al. The role of inflammation in the pathogenesis of heart failure[J]. Curr Cardiol Rep, 2002, 4(3):200-205.

[4] Aukrust P, Yndestad A, Damas JK. Therapeutic potential of anticytokine therapy in congestive heart failure[J]. Am J Cardiovasc Drugs, 2004, 4(3):169-177.

[5] Kai H, Kuwahara F, Tokuda K, et al. Diastolic dysfunction in hypertensive hearts: roles of perivascular inflammation and reactive myocardial fibrosis[J]. Hypertens Res, 2005, 28(6):483-490.

[6] Hayashidani S, Tsutsui H, Shiomi T, et al. Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction[J]. Circulation, 2003, 108(17):2134-2140.

[7] Niu J, Azfer A, Kolattukudy PE. Monocyte-specific Bcl-2 expression attenuates inflammation and heart failure in monocyte chemoattractant protein-1 (MCP-1)-induced cardiomyopathy[J]. Cardiovasc Res, 2006, 71(1):139-148.

[8] Zhou L, Azfer A, Niu J, et al. Monocyte chemoattractant protein-1 induces a novel transcription factor that causes cardiac myocyte apoptosis and ventricular dysfunction[J]. Circ Res, 2006, 98(9):1177-1185.

备注/Memo

备注/Memo:
收稿日期:2008-7-9.通讯作者:蒋学俊,主任医师,主要从事心脏电生理与介入心脏病学研究Email:xjjiang@yahoo.com 作者简介:彭彬,主治医师,硕士Email:boshipb@163.com
更新日期/Last Update: 2009-07-22