Copyright © 1995 by the European Society of Cardiology.
© 1995 The European Society of Cardiology
Depressed unloaded sarcomere shortening velocity in acute murine coxsackievirus myocarditis: myocardial remodeling in the absence of necrosis or hypertrophy
Departments of Molecular Physiology and Biophysics Burlington, Vermont, U.S.A.
* Pathology, College of Medicine, University of Vermont Burlington, Vermont, U.S.A.
Burt B. Hamrell, Department of Molecular Physiology and Biophysics, College of Medicine, UVM Medical Research Facility, 55A South Park Drive. Colchester. VT 05446-2500, U.S.A.
We used right ventricular papillary muscles to study cellular dysfunction in acute murine coxsackievirus myocarditis. We measured unloaded sarcomere shortening velocity (V0) with laser diffraction (HeNe,
=623-8 nm) 7 days after coxsackie virus infection (M) (n = 7) and after infection + monoclonal antibodies to eliminate T cells (T) (n = 4) and in normals (N) (n = 8). A servomotor rapidly shortened a muscle until slack early in contraction and V0 was measured at the onset of zero force. V0 in N was 414 ± 0.84 µS-1 at SI = 208 ± 009 µm, 1.70 ± 0.33 µm.s-1 at 2.06 ± 0.08 µm in M and, in preliminary experiments, 4.75 ± 0.96 µm.s-1 at 2.06 ± 0.07 µm in T. Resting force and stiffness were normal in M. Ventriculor weights in M and T were the same as N. There was an increase in mononudear cells in M papillary muscles, but no fibrosis or necrosis. Thus, V0 was markedly reduced in acute viral myocarditis in the absence of tissue disruption or hypertrophy, but not if T cells were absent. Pyrophosphate gel electrophoresis showed a shift from predominantly fast in N to a slow myosin isoform in M. Myosin remodelling and reduced unloaded sarcomere shortening velocity occur early in acute coxsackievirus myocarditis and are dependent on immune responses to the virus, but are not a result of histopathological changes.
Key Words: Myocarditis sarcomere shortening velocity diffraction heart myocardial papillary muscle myosin isozyme