Received March 9, 2004
Revised June 15, 2004
Accepted after revision June 29, 2004

¹ University of Auckland
² Massachusetts Institute of Technology

^* To whom correspondence should be addressed. E-mail: r.kirton{at}auckland.ac.nz.

	Abstract

Strain softening is commonly reported during mechanical testing of passive whole hearts. It is typically manifested as a stiffer force-extension relation in the first deformation cycle relative to subsequent cycles and is distinguished from viscoelasticity by a lack of recovery of stiffness, even after several hours of rest. The cause of this behaviour is currently unknown. In order to investigate its origins, we have subjected trabeculae to physiologically realistic extensions (5% to 15% of muscle length at 26°C and 0.5 mM Ca2+), while measuring passive force and dynamic stiffness. Whereas we did not observe strain softening in viable trabeculae, we found that it was readily apparent in non-viable (electrically inexcitable) trabeculae undergoing the same extensions. This result was obtained in both the presence and absence of 2,3-butanedione monoxime (BDM). Furthermore, BDM had no effect on the passive compliance of viable specimens, while its presence partially inhibited, but could not prevent, stiffening of non-viable specimens. Loss of viability was accompanied by a uniform increase of dynamic stiffness over all frequencies examined (0.2 - 100 Hz). The presence of strain softening during length extensions of non-viable tissue resulted in a comparable uniform decrease of dynamic stiffness. It is therefore concluded that strain softening is neither intrinsic to viable rat RV trabeculae nor influenced by BDM but, rather, reflects irreversible damage of tissue in partial, or full, rigor.

Key Words: Cardiac muscle, Rat, Stress