Papillary muscles from cats with experimentally induced heart failure and ventricular hypertrophy exhibited decreased maximum velocity of shortening and tension development.
Does experimentally produced ventricular hypertrophy and heart failure alter the intrinsic contractile state of cardiac muscle in cats?
Congestive heart failure and ventricular hypertrophy are associated with an intrinsic depression of myocardial contractility per unit of muscle, even before overt failure occurs.
The contractile state of papillary muscles from hypertrophied and from failing right ventricles of cats with pulmonary artery constriction was studied. In muscles from failing hearts, the maximum velocity of shortening, active length-tension curves, and maximum rate of tension development were decreased, while the passive length-tension curves and the time from stimulation to peak tension were normal. The augmentation of isometric tension achieved by paired electrical stimulation, increasing frequency of contraction, and strophanthidin was reduced. In muscle from hearts without failure but with ventricular hypertrophy, there were qualitatively similar depressions of contractile function, although of lesser magnitude. It is concluded that congestive heart failure is associated with extreme quantitative abnormalities of the intrinsic contractile state of each unit of heart muscle, which reflect a depression in the intensity of the active state. Further, ventricular hypertrophy in the absence of failure is associated with a depression of the contractility of each unit of myocardium, while cardiac compensation is maintained by the increase in muscle mass.
Spann et al. (Fri,) conducted a other in Ventricular hypertrophy and heart failure. Pulmonary artery constriction (experimental model) vs. Normal contractile function (implied) was evaluated on Contractile state of papillary muscles (maximum velocity of shortening, active length-tension curves, maximum rate of tension development). Papillary muscles from cats with experimentally induced heart failure and ventricular hypertrophy exhibited decreased maximum velocity of shortening and tension development.