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1 Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina and the Ralph H. Johnson Department of Veterans Affairs Medical Center, Charleston 29401; and 2 Cardiothoracic Surgery Division, Department of Surgery, Medical University of South Carolina, Charleston, South Carolina 29425
To determine whether and to what extent one component of the extracellular matrix, fibrillar collagen, contributes causally to abnormalities in viscoelasticity, collagen was acutely degraded by activation of endogenous matrix metalloproteinases (MMPs) with the serine protease plasmin. Papillary muscles were isolated from normal cats and cats with right ventricular pressure overload hypertrophy (POH) induced by pulmonary artery banding. Plasmin treatment caused MMP activation, collagen degradation, decreased the elastic stiffness constant, and decreased the viscosity constant in both normal and POH muscles. Thus, whereas many mechanisms may contribute to the abnormalities in myocardial viscoelasticity in the POH myocardium, changes in fibrillar collagen appear to play a predominant role.
matrix metalloproteinases; muscle; stiffness; viscosity
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