Plasmin treatment decreased the elastic stiffness and viscosity constants in both normal and pressure overload hypertrophied cat myocardium, indicating fibrillar collagen plays a predominant role.
Degradation of fibrillar collagen by plasmin decreases elastic stiffness and viscosity in hypertrophied myocardium, indicating collagen's predominant role in viscoelastic abnormalities.
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.
Stroud et al. (Sat,) conducted a other in Right ventricular pressure overload hypertrophy. Serine protease plasmin vs. Normal cats was evaluated on Viscoelastic properties (elastic stiffness constant and viscosity constant). Plasmin treatment decreased the elastic stiffness and viscosity constants in both normal and pressure overload hypertrophied cat myocardium, indicating fibrillar collagen plays a predominant role.