A model approach to the adaptation of cardiac structure by mechanical feedback in the environment of the cell.
The uniformity of the mechanical load of the cardiac fibers in the wall is maintained by continuous remodeling. In this proposed model the myocyte changes direction in optimizing systolic sarcomere shortening. Early systolic stretch and contractility increases the mass of contractile proteins. Cyclic strain of the myocardial tissue diminishes passive stiffness, resulting in the control of ventricular end-diastolic volume. Utilizing these rules of remodeling in our mathematical model yields that the natural helical pathways of the myocardial fibers in the wall are formed automatically.
Arts
T
T
Department of Biophysics, Cardiovascular Research Institute Maastricht, University of Limburg, The Netherlands.
Prinzen
F W
FW
Snoeckx
L H
LH
Reneman
R S
RS
D000222:Adaptation, Physiological; D000818:Animals; D005246:Feedback; D006321:Heart / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009200:Myocardial Contraction / Q000502:physiology*; D013314:Stress, Mechanical