A mechanical model for adjustable passive stiffness in rabbit detrusor
John E Speich1, Kevin Quintero, Christopher Dosier
1Department of Mechanical Engineering, Virginia Commonwealth University, 601 West Main St., P. O. Box 843015, Richmond, 23284-3015, USA. jespeich@vcu.edu
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 17, 2006
Summary
Rabbit detrusor smooth muscle (DSM) shows adjustable passive stiffness. Its stiffness history, including strain and activation, reversibly alters mechanical properties, explained by a new cross-linking model.
Area of Science:
- Physiology
- Biomechanical Engineering
- Smooth Muscle Physiology
Background:
- Detrusor smooth muscle (DSM) exhibits strain softening, a decrease in stiffness after stretching, distinct from viscoelasticity.
- This phenomenon is linked to cross-link dynamics, being irreversible in passive muscle but reversible upon activation.
Purpose of the Study:
- To investigate the history-dependent adjustable passive stiffness of rabbit detrusor smooth muscle.
- To provide empirical data and propose a mechanical model explaining strain softening reversibility.
Main Methods:
- Experimental analysis of passive isometric force relaxation in rabbit DSM over extended periods.
- Application of quick-release protocols to assess force redevelopment and relaxation dynamics.
- Development of a mechanical model incorporating a novel cross-linking element into a hybrid Kelvin/Voigt viscoelastic framework.
Main Results:
- Passive isometric force relaxation in DSM includes a slow component lasting hours.
- Previously strain-softened DSM maintains less steady-state passive force.
- Quick-release protocols reveal a biphasic response: force redevelopment followed by relaxation.
Conclusions:
- Detrusor smooth muscle possesses adjustable passive stiffness influenced by strain and activation history.
- A proposed mechanical model, including a novel cross-linking element, can explain these observed phenomena.
- Understanding these properties is crucial for bladder function and dysfunction research.


