Effects of metoprolol treatment on a disintegrin metalloproteinase expression and extracellular matrix remodeling after myocardial infarction in rats  

作　　者：ZHAO Juan QU Xiu-fen ZHAO Chun-yu CAO Feng-lin ZHOU Tao LI Wei-min HUANG Yong-lin 

机构地区：[1]Department of Cardiology, First Affiliated Hospital of HarbinMedical University, Harbin 150001, China [2]Department of Neurological Rehabilitation, China RehabilitationResearch Center, Beijing 100068, China [3]Laboratory of Cardiology, First Affiliated Hospital of HarbinMedical University, Harbin 150001, China [4]Da＇an Living Limited Company, Sun Yat-sen University,Guangzhou 510070, China

出　　处：《Chinese Medical Journal》2007年第17期1549-1552,共4页中华医学杂志（英文版）

基　　金：This work was supported by the grants from the National Natural Science Foundation of Chian(No.30470687);Heilongjiang Doctorate Foundation grant(No.SCX2005020)

摘　　要：Ventricular remodeling （VR） after myocardial infarction （MI） makes a full impact on left ventricular dilation and dysfunction, severe arrhythmias and even sudden death. Thus it is very interesting and instructive to study the underlying regulatory mechanism for VR. Recently, evidenceI suggests that tumor necrosis factor-α （TNF-α） activity can independently influence VR, and aggravate myocardial dysfunction and cell death in the ventricle. The activation of pro-TNF〈t is adjusted by a disintegrin metalloproteinase （ADAM） 10 and ADAM17, the latter might take part in extracellular matrix （ECM） modulation in the borderline region of cardiac infarction.2 However, little is known about the relationship between ADAMsl0, 17 expressions and TNF-α activity in the process of VR after MI. The present study tested the hypothesis in rats that the interaction between ADAMsl0, 17 expressions and TNF-α activity was a contributory mechanism for VR of the healing myocardium, and metoprolol treatment might ameliorate VR inhibiting the mechanism.Ventricular remodeling （VR） after myocardial infarction （MI） makes a full impact on left ventricular dilation and dysfunction, severe arrhythmias and even sudden death. Thus it is very interesting and instructive to study the underlying regulatory mechanism for VR. Recently, evidenceI suggests that tumor necrosis factor-α （TNF-α） activity can independently influence VR, and aggravate myocardial dysfunction and cell death in the ventricle. The activation of pro-TNF〈t is adjusted by a disintegrin metalloproteinase （ADAM） 10 and ADAM17, the latter might take part in extracellular matrix （ECM） modulation in the borderline region of cardiac infarction.2 However, little is known about the relationship between ADAMsl0, 17 expressions and TNF-α activity in the process of VR after MI. The present study tested the hypothesis in rats that the interaction between ADAMsl0, 17 expressions and TNF-α activity was a contributory mechanism for VR of the healing myocardium, and metoprolol treatment might ameliorate VR inhibiting the mechanism.

关 键 词：myocardial infarction a disintegrin metalloproteinase extracellular matrix ventricular remodeling METOPROLOL 

分 类 号：R54[医药卫生—心血管疾病]