Evaluation of fundamental hypotheses underlying constrained mixture models of arterial growth and remodelling

Andreas Valentin1, Jay D. Humphrey1
1Department of Biomedical Engineering, 337 Zachry Engineering Center, 3120 TAMU, Texas A&M University, College Station, TX 77843-3120, USA

Tóm tắt

Evolving constituent composition and organization are important determinants of the biomechanical behaviour of soft tissues. In arteries, vascular smooth muscle cells and fibroblasts continually produce and degrade matrix constituents in preferred modes and at altered rates in response to changing mechanical stimuli. Smooth muscle cells similarly exhibit vasoactive changes that contribute to the control of overall structure, function and mechanical behaviour. Constrained mixture models provide a useful framework in which to quantify arterial growth and remodelling for they can account for cell-mediated changes in individual structurally significant constituents. Our simulations show that the combined effects of changing mass density turnover and vasoactivity, as well as the prestretch at which constituents are incorporated within extant matrix, are essential to capture salient features of bounded arterial growth and remodelling. These findings emphasize the importance of formulating biologically motivated constitutive relations in any theory of growth and remodelling and distinct advantages of the constrained mixture approach, in particular.

Từ khóa


Tài liệu tham khảo

Alberts B., 2002, The molecular biology of the cell, 4

10.1007/s10237-007-0101-2

10.1080/10255840601160484

10.1115/1.2132374

10.1007/s10439-007-9322-x

Cardamone L., Origin of axial prestretch and residual stress in arteries, Biomech. Model. Mechanobiol., 0237

10.1161/01.RES.76.2.168

Dajnowiec D.& Langille B. L.. 2007 Arterial adaptations to chronic changes in haemodynamic function: coupling vasomotor tone to structural remodelling. 113 15–23. (doi:10.1042/CS20060337).

10.1152/physrev.1995.75.3.519

10.1016/j.freeradbiomed.2007.04.017

10.1002/bip.1977.360160604

10.1016/j.jtbi.2003.08.004

10.1243/0954411981533854

10.1152/ajpheart.2001.280.6.H2752

10.1007/BF02584301

10.1159/000080699

10.1016/j.jbiomech.2004.06.017

10.1115/1.1762899

Guyton A. C., 1997, Human physiology and mechanisms of disease, 6

10.1007/s10237-006-0049-7

10.1023/A:1010835316564

10.1007/978-0-387-21576-1

10.1007/s12013-007-9002-3

10.1161/HYPERTENSIONAHA.107.103440

10.1142/S0218202502001714

10.1146/annurev.bioeng.10.061807.160439

10.1016/S0021-9290(03)00178-7

10.1161/01.RES.0000016481.87703.CC

10.1016/S0070-2153(04)62006-0

10.1002/jcp.20546

10.1007/s10237-006-0062-x

10.1097/00005344-199321001-00003

10.1139/y96-082

10.1016/0021-9290(83)90041-6

10.1126/science.128820

10.1159/000025570

10.1007/s10237-006-0061-y

10.1038/ncb1216

10.1073/pnas.12.3.207

10.1007/s10439-008-9438-7

10.1016/0531-5565(77)90001-8

10.1073/pnas.75.1.451

10.1161/01.HYP.36.3.319

Price J. M., 1981, Length-dependent sensitivity in vascular smooth muscle, Am. J. Physiol., 241, HS57

10.1023/A:1010800703478

10.1114/1.191

10.1115/1.2834313

10.1006/jtbi.2000.2143

10.1006/jmcc.1996.0480

10.1006/jmcc.1996.0023

10.1159/000169701

10.1016/0021-9290(94)90021-3

Ruch T. C., 1966, Physiology and biophysics, 19

10.1007/978-94-009-7538-5_23

10.1159/000081972

10.1016/j.pbiomolbio.2007.07.025

10.1146/annurev.physiol.59.1.89

10.1073/pnas.111133298

10.1115/1.2798001

10.1152/ajpheart.00684.2007

10.1098/rsif.2008.0254

10.1007/s10439-007-9375-x

10.1083/jcb.123.3.741

10.1161/01.RES.26.4.507

10.1085/jgp.69.4.449

10.1152/ajpheart.00094.2004