Biophysical Journal 66: 953-961 (1994)
© 1994 the Biophysical Society

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Arts, T Articles by Reneman, R S Search for Related Content PubMed PubMed Citation Articles by Arts, T Articles by Reneman, R S

Adaptation of cardiac structure by mechanical feedback in the environment of the cell: a model study.

Department of Biophysics, Cardiovascular Research Institute Maastricht (CARIM), University of Limburg, The Netherlands.

ABSTRACT

In the cardiac left ventricle during systole mechanical load of the myocardial fibers is distributed uniformly. A mechanism is proposed by which control of mechanical load is distributed over many individual control units acting in the environment of the cell. The mechanics of the equatorial region of the left ventricle was modeled by a thick-walled cylinder composed of 6-1500 shells of myocardial fiber material. In each shell a separate control unit was simulated. The direction of the cells was varied so that systolic fiber shortening approached a given optimum of 15%. End-diastolic sarcomere length was maintained at 2.1 microns. Regional early-systolic stretch and global contractility stimulated growth of cellular mass. If systolic shortening was more than normal the passive extracellular matrix stretched. The design of the load-controlling mechanism was derived from biological experiments showing that cellular processes are sensitive to mechanical deformation. After simulating a few hundred adaptation cycles, the macroscopic anatomical arrangement of helical pathways of the myocardial fibers formed automatically. If pump load of the ventricle was changed, wall thickness and cavity volume adapted physiologically. We propose that the cardiac anatomy may be defined and maintained by a multitude of control units for mechanical load, each acting in the cellular environment. Interestingly, feedback through fiber stress is not a compelling condition for such control.

This article has been cited by other articles:

				M.-T. Wu, W.-Y. I. Tseng, M.-Y. M. Su, C.-P. Liu, K.-R. Chiou, V. J. Wedeen, T. G. Reese, and C.-F. Yang Diffusion Tensor Magnetic Resonance Imaging Mapping the Fiber Architecture Remodeling in Human Myocardium After Infarction: Correlation With Viability and Wall Motion Circulation, September 5, 2006; 114(10): 1036 - 1045. [Abstract] [Full Text] [PDF]

				T. Arts, T. Delhaas, P. Bovendeerd, X. Verbeek, and F. W. Prinzen Adaptation to mechanical load determines shape and properties of heart and circulation: the CircAdapt model Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1943 - H1954. [Abstract] [Full Text] [PDF]

				C. E. Miller, C. L. Wong, and D. Sedmera Pressure overload alters stress-strain properties of the developing chick heart Am J Physiol Heart Circ Physiol, November 1, 2003; 285(5): H1849 - H1856. [Abstract] [Full Text] [PDF]

				A. Van der Toorn, P. Barenbrug, G. Snoep, F. H. Van der Veen, T. Delhaas, F. W. Prinzen, J. Maessen, and T. Arts Transmural gradients of cardiac myofiber shortening in aortic valve stenosis patients using MRI tagging Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1609 - H1615. [Abstract] [Full Text] [PDF]

				M. Vendelin, P. H. M. Bovendeerd, J. Engelbrecht, and T. Arts Optimizing ventricular fibers: uniform strain or stress, but not ATP consumption, leads to high efficiency Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1072 - H1081. [Abstract] [Full Text] [PDF]

				L. Geerts, P. Bovendeerd, K. Nicolay, and T. Arts Characterization of the normal cardiac myofiber field in goat measured with MR-diffusion tensor imaging Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H139 - H145. [Abstract] [Full Text] [PDF]

				M. F.M van Oosterhout, T. Arts, J. B Bassingthwaighte, R. S Reneman, and F. W Prinzen Relation between local myocardial growth and blood flow during chronic ventricular pacing Cardiovasc Res, March 1, 2002; 53(4): 831 - 840. [Abstract] [Full Text] [PDF]

				T. Arts, K. D. Costa, J. W. Covell, and A. D. McCulloch Relating myocardial laminar architecture to shear strain and muscle fiber orientation Am J Physiol Heart Circ Physiol, May 1, 2001; 280(5): H2222 - H2229. [Abstract] [Full Text] [PDF]

				W.-Y. I. Tseng, T. G. Reese, R. M. Weisskoff, T. J. Brady, and V. J. Wedeen Myocardial Fiber Shortening in Humans: Initial Results of MR Imaging Radiology, July 1, 2000; 216(1): 128 - 139. [Abstract] [Full Text]

				D. F. Scollan, A. Holmes, R. Winslow, and J. Forder Histological validation of myocardial microstructure obtained from diffusion tensor magnetic resonance imaging Am J Physiol Heart Circ Physiol, December 1, 1998; 275(6): H2308 - H2318. [Abstract] [Full Text] [PDF]

				M. F. M. van Oosterhout, F. W. Prinzen, T. Arts, J. J. Schreuder, W. Y. R. Vanagt, J. P. M. Cleutjens, and R. S. Reneman Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall Circulation, August 11, 1998; 98(6): 588 - 595. [Abstract] [Full Text] [PDF]

				J. H. Omens, T. P. Usyk, Z. Li, and A. D. McCulloch Muscle LIM protein deficiency leads to alterations in passive ventricular mechanics Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H680 - H687. [Abstract] [Full Text] [PDF]