Key Points
- To assess the mechanical properties of contractile and series elastic elements in hypertrophied cardiac muscle in the absence of congestive heart failure.
- Examined isolated right ventricular papillary muscles from normal rabbits and rabbits with sustained pulmonary artery constriction causing a 67% reduction in external diameter.
- Obtained instantaneous force-velocity data at 30% to 38% of time to peak tension across resting muscle lengths of 96%, 98%, and 100% of optimal length.
- Calculated unloaded shortening velocity (Vmax) using a linearized form of the Hill hyperbolic equation.
- Unloaded shortening velocity (Vmax) was depressed by 36% in hypertrophied cardiac muscle compared to normal controls.
- Shortening velocity did not vary with muscle length in either normal or hypertrophied muscles, indicating a length- and time-independent depression of contractile element capacity.
Structured PICO
PPopulationRight ventricular papillary muscles from normal rabbits and rabbits with sustained pulmonary artery constriction (67% decrease in external diameter)
IInterventionSustained pulmonary artery constriction (hypertrophy model)
OOutcomeUnloaded shortening velocity (Vmax) and instantaneous force-velocity datasurrogate
Hypertrophied rabbit cardiac muscle exhibits a length- and time-independent depression of contractile element shortening capacity, consistent with depressed ATPase activity.