摘要篇首： 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, evidence1 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-a 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 ADAMs10, 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 ADAMs10, 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.