title: Mechanics of active contraction in cardiac muscle: Part II--Cylindrical models of the systolic left ventricle.
abstract: Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general "deactivation" model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying "elastance" model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a "Hill" model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 microns less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.
authors.affiliation: Department of Biomedical Engineering, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205.
authors.forename: J M
authors.initials: JM
authors.lastname: Guccione
authors.forename: L K
authors.initials: LK
authors.lastname: Waldman
authors.forename: A D
authors.initials: AD
authors.lastname: McCulloch
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D002118:Calcium / Q000502:physiology; D004285:Dogs; D004548:Elasticity; D004594:Electrophysiology; D005069:Evaluation Studies as Topic; D005544:Forecasting; D006439:Hemodynamics; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D012212:Rheology; D012518:Sarcomeres / Q000187:drug effects / Q000502:physiology*; D013314:Stress, Mechanical; D013318:Stroke Volume; D013599:Systole / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
chemical_list: D002118:Calcium