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|本期目录/Table of Contents|

阿替洛尔对小鼠心肌肥厚干预作用的研究

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2013年第3期
页码:
317-322
栏目:
基础研究
出版日期:
2013-06-25

文章信息/Info

Title:
Effect of atenolol on cardiac hypertrophy in mice
作者:
刘宝辉1; 李明凯2; 党海舟1; 徐 明3; 罗晓星2; 俞世强1
(第四军医大学：1.西京医院心血管外科，2.药学院药理学教研室，3.基础医学院生理学教研室，陕西 西安 710032)
Author(s):
LIU Baohui1;  LI Mingkai2;  DANG Haizhou1;  XU Ming3;  LUO Xiaoxing2;  YU Shiqiang1
(1.Department of Cardiovascular Surgery, Xijing Hospital, 2.Department of Pharmacology, School of Pharmacy, Fourth Military Medical University, 3.Department of Physiology, School of Basic Medical Science, Xi’an 710032, Shaanxi, China)
关键词:
阿替洛尔; 主动脉弓缩窄术; 心肌肥厚; 小鼠
Keywords:
aortic arches constriction;  pressure overload;  left ventricular hypertrophy;  atenolol
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的:观察β1受体阻滞剂阿替洛尔(atenolol，ATE)对主动脉弓缩窄术(aortic arches constriction，AAC)诱导的C57BL小鼠心肌肥厚模型的治疗作用。方法:通过AAC建立心肌肥厚小鼠模型，将24只雄性C57BL小鼠随机分为正常对照组、假手术(Sham)组、AAC组和AAT+ATE组，每组6只小鼠(n=6)。给予ATE 4周后，进行心脏超声检查，并测量心脏质量/体质量（HW/BW）、左心室质量/体质量(LVW/BW)、左室舒张末期内径（LVEDD)、左室收缩末期内径(LVEDS)、左室射血分数［LVEF(%)］和短轴缩短率［FS(%)］。应用PCR检测心肌组织中心房钠尿肽(ANP)、脑尿钠肽(BNP)和肌球蛋白重链(α-MHC)基因表达的水平，并行病理学检查。结果： 与AAC组比较，正常对照组、Sham组和AAC+ATE组的LVEDD分别降低24.9%、17.7%和18.2%，LVEDS分别降低32.9%、34.1%和26.3%；LVEF(%)分别提高65.6%、75.8%和49.5%，FS(%)分别提高79.7%、100.0%和62.6%（均P<0.05）；AAC+ATE组与AAC组相比，LVM/BW和心肌细胞平均横截面积均明显降低（P<001）；而与正常对照组相比，细胞平均面积明显增大（P<0.05）。AAC+ATE组中ANP、BNP和α-MHC的表达水平显著低于AAC组（P<0.05）。结论:通过阻断β1受体ATE，可以对压力超负荷等原因诱导的心肌肥厚发挥治疗作用。
Abstract:
AIM:To observe the effect of β1receptor blocker, atenolol, on transverse aortic constriction (AAC)induced myocardial hypertrophy. METHODS: Twentyfour male C57BL mice were randomly divided into four groups: normal control group, sham group, AAC operation group and AAC plus atenolol treatment group. After four weeks' treatment, echocardiogram was performed to assess the cardiac function changes, heart weight to body weight ratio (HW/BW), heart weight/tibial length, left ventricular ejection fraction ［LVEF(%)］ and LV fractional shortening ［FS(%)］. The expression levels of ANP, BNP and βMHC mRNAs in heart tissues and the size of cardiomyocytes were also measured using PCR and pathological techniques. RESULTS: Compared with those in AAC group, LVEDd decreased 249%, 177% and 182% and LVEDs decreased 329%, 341% and 263%, respectively in normal control group, sham group and atenolol group, while EF increased 656%, 758% and 495%, and FS increased 797%, 1000% and 626%, respectively (P<005). The LVM/BW and the cardiac myocyte crosssectional area showed a decrease in atenolol group compared with that in AAC group (P<001), but they still increased significantly compared with those in normal control group. The expression of ANP, BNP and αMHC mRNAs in atenolol group were lower than those in AAC group (P<005). CONCLUSION: Atenolol can intervene the progress of pressure overloadinduced myocardial hypertrophy in C57BL mice.

参考文献/References

[1]Kucukler N,Kurt IH,Topaloglu C,et al.The effect of valsartan on left ventricular myocardial functions in hypertensive patients with left ventricular hypertrophy[J].J Cardiovasc Med (Hagerstown),2012,13(3):181-186.
[2]Banerjee I,Avatapalle B,Petkar A,et al.The association of cardiac ventricular hypertrophy with congenital hyperinsulinism[J].Eur J Endocrinol,2012,167(5):619-624.
[3]Yano M,Kim S,Izumi Y,et al.Differential activation of cardiac cjun aminoterminal kinase and extracellular signalregulated kinase in angiotensin IImediated hypertension[J].Circ Res,1998,83(7):752-760.
[4]Kuwahara K,Nishikimi T,Nakao K.Transcriptional regulation of the fetal cardiac gene program[J].J Pharmacol Sci,2012,119(3):198-203.
[5]arry SP,Davidson SM,Townsend PA.Molecular regulation of cardiac hypertrophy[J].Int J Biochem Cell Biol,2008,40(10):2023-2039.
[6]Shimano M,Ouchi N,Nakamura K,et al.Cardiac myocyte follistatinlike 1 functions to attenuate hypertrophy following pressure overload[J].Proc Natl Acad Sci U S A,2011,108(43):E899-E906.
[7]Hudson B,Hidalgo C,Saripalli C,et al.Hyperphosphorylation of mouse cardiac titin contributes to transverse aortic constrictioninduced diastolic dysfunction[J].Circ Res,2011,109(8):858-866.
[8]丁学亮,朱烨静,尹新华.Wnt信号通路在心肌肥厚中作用的研究进展[J].心脏杂志,2012,24(3):411-415.
[9]Sala V,Gallo S,Leo C,et al.Signaling to Cardiac Hypertrophy:Insights from Human and Mouse RASopathies[J].Mol Med,2012, 18(9):938-947.
[10]Dickstein K,Cohen Solal A,Filippatos G,et al.ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine(ESICM)[J].Eur J Heart Fail,2008,10(10):933-989.
[11]党海舟,李明凯,徐 明,等.主动脉弓缩窄术和腹腔注射IPH致小鼠慢性心衰两种模型的比较和评价[J].心脏杂志,2012,24(2):168-172.
[12]Chen J,Wu J,Li L,et al.Effect of an acute mechanical stimulus on aortic structure in the transverse aortic constriction mouse model[J].Clin Exp Pharmacol Physiol,2011,38(9):570-576.
[13]McDermott PJ,Baicu CF,Wahl SR,et al.In vivo measurements of the contributions of protein synthesis and protein degradation in regulating cardiac pressure overload hypertrophy in the mouse[J].Mol Cell Biochem,2012,367(1-2):205-213.
[14]Musumeci M,Maccari S,Corritore E,et al.Signaling pathwayfocused gene expression profiling in pressure overloaded hearts[J].Ann Ist Super Sanita,2011,47(3):290-295.

备注/Memo

备注/Memo:
收稿日期：2012-11-22.
基金项目：国家自然科学基金资助课题（81070198，30800310）
通讯作者：罗晓星，教授，主要从事心脏组胺生理病理学研究Email：xxluo3@fmmu.edu.cn 共同通讯作者：俞世强，主任医师，主要从事微创心脏外科研究Email：yushiq@fmmu.edu.cn
作者简介：刘宝辉，硕士生Email：liubaohui520@126.com
更新日期/Last Update: 2013-07-16