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本文引用的文献

1
Origin of axial prestretch and residual stress in arteries.动脉轴向预拉伸和残余应力的起源。
Biomech Model Mechanobiol. 2009 Dec;8(6):431-46. doi: 10.1007/s10237-008-0146-x.
2
Complementary vasoactivity and matrix remodelling in arterial adaptations to altered flow and pressure.动脉对血流和压力改变的适应性过程中的互补性血管活性与基质重塑
J R Soc Interface. 2009 Mar 6;6(32):293-306. doi: 10.1098/rsif.2008.0254.
3
Intracranial and abdominal aortic aneurysms: similarities, differences, and need for a new class of computational models.颅内和腹主动脉瘤:异同点及对新型计算模型的需求
Annu Rev Biomed Eng. 2008;10:221-46. doi: 10.1146/annurev.bioeng.10.061807.160439.
4
Mechanisms of arterial remodeling in hypertension: coupled roles of wall shear and intramural stress.高血压中动脉重塑的机制:壁面剪切力与壁内应力的协同作用
Hypertension. 2008 Aug;52(2):195-200. doi: 10.1161/HYPERTENSIONAHA.107.103440. Epub 2008 Jun 9.
5
Time-dependent changes in smooth muscle cell stiffness and focal adhesion area in response to cyclic equibiaxial stretch.响应周期性等双轴拉伸时平滑肌细胞硬度和粘着斑面积随时间的变化。
Ann Biomed Eng. 2008 Mar;36(3):369-80. doi: 10.1007/s10439-008-9438-7. Epub 2008 Jan 24.
6
Vascular adaptation and mechanical homeostasis at tissue, cellular, and sub-cellular levels.组织、细胞和亚细胞水平的血管适应性与机械稳态。
Cell Biochem Biophys. 2008;50(2):53-78. doi: 10.1007/s12013-007-9002-3. Epub 2007 Oct 24.
7
Smooth muscle contraction: mechanochemical formulation for homogeneous finite strains.平滑肌收缩:均匀有限应变的机械化学公式
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8
Arterial remodeling in response to hypertension using a constituent-based model.使用基于成分的模型研究高血压引起的动脉重塑。
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10
Increased proteolysis of collagen in an in vitro tensile overload tendon model.体外拉伸过载肌腱模型中胶原蛋白蛋白水解增加。
Ann Biomed Eng. 2007 Nov;35(11):1961-72. doi: 10.1007/s10439-007-9375-x. Epub 2007 Sep 1.

动脉生长与重塑的约束混合模型基础假设的评估

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

作者信息

Valentín A, Humphrey J D

机构信息

Department of Biomedical Engineering, 337 Zachry Engineering Center, 3120 TAMU, Texas A&M University, College Station, TX 77843-3120, USA.

出版信息

Philos Trans A Math Phys Eng Sci. 2009 Sep 13;367(1902):3585-606. doi: 10.1098/rsta.2009.0113.

DOI:10.1098/rsta.2009.0113
PMID:19657012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2865879/
Abstract

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.

摘要

不断演变的成分组成和组织结构是软组织生物力学行为的重要决定因素。在动脉中,血管平滑肌细胞和成纤维细胞会根据不断变化的机械刺激,以特定模式并以变化的速率持续产生和降解基质成分。平滑肌细胞同样会表现出血管活性变化,这有助于控制整体结构、功能和机械行为。约束混合模型提供了一个有用的框架,用于量化动脉生长和重塑,因为它们可以解释细胞介导的个体结构重要成分的变化。我们的模拟表明,质量密度周转和血管活性变化的综合影响,以及成分在现有基质中嵌入时的预拉伸,对于捕捉有界动脉生长和重塑的显著特征至关重要。这些发现强调了在任何生长和重塑理论中制定具有生物学动机的本构关系的重要性,特别是约束混合方法的独特优势。