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|

缬沙坦对压力超负荷下兔左室心肌TNF-α表达及胶原重构的影响 (PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2004年第1期
页码:
33-36
栏目:
实验研究
出版日期:
2004-01-01

文章信息/Info

Title:
Effect of Valsartan on TNF-α expression and collagen remodeling in left ventricle of rabbit undergoing pressure overload
作者:
王军奎; 崔长琮; 姚晓伟; 崔翰斌; 姚青海
西安交通大学第一医院心内科,陕西 西安 710061
Author(s):
WANG Jun-kui; CUI Chang-cong; YAO Xiao-wei; CUI Han-bin; YAO Qing-hai
Department of Cardiology, First Hospital, Xi'an Jiotong University, Xi'an, Shaanxi 710061 China
关键词:
缬沙坦; 胶原纤维; 心室重构; 肿瘤坏死因子-α
Keywords:
Valsartan;  collagen fibers;  ventricular remodeling;  tumor necrosis factor-α
分类号:
R341.1
DOI:
-
文献标识码:
A
摘要:
目的: 观察缬沙坦(Valsartan)对慢性压力超负荷下左室心肌 TNF-α表达、胶原重构及心功能的影响。方法:家兔30只随机分为假手术组、腹主动脉次全结扎组(简称结扎组)、缬沙坦干预结扎组(简称干预组),每组 10只。术后 12周进行血流动力学检查并取左室心肌行VG染色及免疫组化染色分别观察胶原容积百分比(CVF)及TNF-α表达情况。结果:结扎组与假手术组比较,TNF-α表达显著增强(P<0.01),左室质量/体质量(LVW/BW)、左室舒张末压(LVEDP)、含小血管视野的CVF(CVF-V)及不含小血管视野的 CVF(CVF-NV)均显著升高(均 P<0.01);缬沙坦干预组与结扎组比较,TNFα表达显著减弱(P<0.01),LVW/BW、LVEDP、CVF-V,CVF-NV显著降低(均 P<0.01)。结论:缬沙坦可抑制压力负荷下心室肌 TNF-α的过度表达并减轻心室肌的胶原增生、心室重构及心功能的损害。
Abstract:
AIM:To study the effect of Valsartan on TNF-αexpression and collagen remodeling in the left ventricle of the rabbit undergoing chronic pressure overload. METHODS: Thirty rabbits were randomly devided into 3 groups (n=10),as the sham operation group, the abdominal aorta banded group(banded group), and the abdominal aorta banded+Valsartan group(Valsartan group). Twele weeks after the operation, hemodynamic parameters were acquired, then collagen volume fraction(CVF) and TNF-α expression of the left ventricle were measure by using VG and immunohistochemical staining. RESULTS: Compare with the sham operation group, TNF-αexpression was enhanced and LVW/BW, LVEDP, CVF-V CVF-NV decreased significantly in the banded group(P< 0.01). Compare with the banded group, TNF-α expression was weakened and LVW/BW, LVEDP, CVF-V, CVF-NV increased significantly in the Valsartan group(P< 001). CONCLUSION: Valsartan can inhibit abnormal TNF-α expression, collagen proliferation, ventricule remodeling in left ventricle of rabbit undergoing chronic pressure overload, thus preserving heart function.

参考文献/References

[1]Sivasubramanian N,Coker ML,Kurrelmyer KM,et al. Left ventricule remodeling intransgenic mice with cardiac restricted overexpression of tumor necrosis factor-α[J]. Circulation, 2001,104(7):826-831.

[2]Li YY,Feng YQ,Kadokami T,et al. Myocardial extracellular matrix remodelingi ntransgenic mice overexpressing tumor necrosis factor α can be modulated by antitumor necrosis factor αtherapy[J]. Proc Natl Acad Sci,2000,97(23):12746-12751.

[3]Nagueh SF,StetsonS J,LakkisN,et al. Decreased expression of tumo rnecrosis factor α and regression of hypertrophy after nonsurgical septal reduction therapy for patients with hypertrophic obstructive cardiomyopathy[J]. Circulation,2001,103(14):1844-1850.

[4]Heberto Herrera GarzaE, Herrera Garza JL,Rodriguez Gonzalez H,et al.Importance of tumor necrosis factor alphain the pathogenesis of heart failure[J]. Rev Esp Cardiol,2002,55(1):61-66.

[5]Meldrum DR.Tumor necrosis factor in the heart[J].Am J Physiol,1998,274(3pt2): R577-R595.

[6]Kapadia SR,Oral H,Lee J, et al. Hemodynamic regulation of tumor necrosis factor-alpha gene and protein expression in adult feline myocardium[J]. Circ Res,1997,81(2):187-195.

[7]Bradham WS,Moe G,Wendt KA,et al.TNF-α and myocardial matrix metalloproteinase in heart failure: relationship to LV remodeling[J]. Am J Physiol,2002,282(4):H1288-H1295.

[8]Peng J,Gurantz D,Tran V,et al. Tumor necrosis factor-α induced AT1 receptor upregulation enhances angiotensin Ⅱ mediated cardiac fibroblast responses that favor fibrosis[J].Circ Res,2002,91(12):1119-1126.

[9]Cohn JN,Tognoni GA.Randomized trial of the angiotensin receptor blocker Valsartan in chronic heart failure[J]. N Engl J Med,2001,354(23):1667-1675.

[10]Yokoyama T,Sekiguchi K,Tanaka T,et al. Angiotensin Ⅱ and mechanical stretch induce production of tumor necrosis factor in cardiac fibroblasts[J]. Am J Physiol,1999,276(6pt2): H1968-H1976.

[11]Kalra D,Sivasubramanian N,Mann DL.Angiotensin Ⅱ induces tumor necrosis factor biosynthesis in the adult mammalian heart through a protein kinase C dependent pathway[J]. Circulation,2002,105(18):2198-2205.

备注/Memo

备注/Memo:
收稿日期：2003-1-20
更新日期/Last Update: 2004-01-01