Growth and remodeling in a thick-walled artery model: effects of spatial variations in wall constituents

Alford, Patrick W.; Humphrey, Jay D.; Taber, Larry A.

doi:10.1007/s10237-007-0101-2

Cited by 146 publications

(127 citation statements)

References 45 publications

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“…Our theoretical model suggests that these phenomena are related by the stress-induced remodeling pathways that endow the vasculature with its robust mechanoadaptability (32,34). Specifically, these results suggest that blast-induced hypercontraction leads to elevated tissue stress, which can, in cases of severe injury, induce maladaptive compensatory remodeling, facilitated by phenotype switching.…”

Section: Discussionmentioning

confidence: 77%

“…We assume that the tissue grows to reequilibrate both tissue stress and basal contraction (32). The relationship between the magnitude of the perturbation from a homeostatic tissue-level target stress and the rate of remodeling _ λ g is given by…”

Section: Methodsmentioning

confidence: 99%

“…where σ o is the tissue's target stress and τ σ and τ a are time constants (32,33,49). We further assume that perturbation from the target stress results in a change in the phenotype population, with small perturbations inducing a more contractile population and large perturbations causing the population to become more synthetic.…”

Section: Methodsmentioning

confidence: 99%

“…Given the reduction in contractile stress at 24 h in the severely injured tissues with respect to both control and mildly injured tissues, we reasoned that severely injured tissues were remodeling their stress state by changing the phenotype of a subpopulation of the VSMCs in the blast-induced hypercontractile tissues. We developed an elasticity-based computational model, based on previous models of stress-induced growth and remodeling (31,32), to better understand how blast-induced hypercontraction potentiates the contractility observed 24 h postblast. The primary assumption of the model is that the tissue has an optimal stress state and actively remodels to return to this target value (33).…”

Section: Dynamic Phenotype Switching Predicts Long-term Contractilitymentioning

confidence: 99%

See 3 more Smart Citations

Blast-induced phenotypic switching in cerebral vasospasm

Alford¹,

Dabiri²,

Goss³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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117

108

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Vasospasm of the cerebrovasculature is a common manifestation of blast-induced traumatic brain injury (bTBI) reported among combat casualties in the conflicts in Afghanistan and Iraq. Cerebral vasospasm occurs more frequently, and with earlier onset, in bTBI patients than in patients with other TBI injury modes, such as blunt force trauma. Though vasospasm is usually associated with the presence of subarachnoid hemorrhage (SAH), SAH is not required for vasospasm in bTBI, which suggests that the unique mechanics of blast injury could potentiate vasospasm onset, accounting for the increased incidence. Here, using theoretical and in vitro models, we show that a single rapid mechanical insult can induce vascular hypercontractility and remodeling, indicative of vasospasm initiation. We employed high-velocity stretching of engineered arterial lamellae to simulate the mechanical forces of a blast pulse on the vasculature. An hour after a simulated blast, injured tissues displayed altered intracellular calcium dynamics leading to hypersensitivity to contractile stimulus with endothelin-1. One day after simulated blast, tissues exhibited blast force dependent prolonged hypercontraction and vascular smooth muscle phenotype switching, indicative of remodeling. These results suggest that an acute, blast-like injury is sufficient to induce a hypercontraction-induced genetic switch that potentiates vascular remodeling, and cerebral vasospasm, in bTBI patients.neurotrauma | mechanotransduction | tissue engineering | vascular mechanics

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Section: Discussionmentioning

confidence: 77%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Dynamic Phenotype Switching Predicts Long-term Contractilitymentioning

confidence: 99%

See 2 more Smart Citations

Blast-induced phenotypic switching in cerebral vasospasm

Alford¹,

Dabiri²,

Goss³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

117

108

View full text Add to dashboard Cite

show abstract

“…In the paper by Alford et al (2008), a mathematical model for growth and remodelling of arteries was presented for a thick-walled tube composed of a constrained mixture of smooth muscle cells, elastin and collagen within the framework developed by Humphrey & Rajagopal (2002) kinematic growth model of Rodriguez et al (1994). Predicted pressure-radius relations and opening angles show reasonable agreement with the experimental results from the literature.…”

Section: (A) Arterial Wall Modelling and Its Applicationsmentioning

confidence: 68%

Constitutive modelling of arteries

2010

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This review article is concerned with the mathematical modelling of the mechanical properties of the soft biological tissues that constitute the walls of arteries. Many important aspects of the mechanical behaviour of arterial tissue can be treated on the basis of elasticity theory, and the focus of the article is therefore on the constitutive modelling of the anisotropic and highly nonlinear elastic properties of the artery wall. The discussion focuses primarily on developments over the last decade based on the theory of deformation invariants, in particular invariants that in part capture structural aspects of the tissue, specifically the orientation of collagen fibres, the dispersion in the orientation, and the associated anisotropy of the material properties. The main features of the relevant theory are summarized briefly and particular forms of the elastic strain-energy function are discussed and then applied to an artery considered as a thickwalled circular cylindrical tube in order to illustrate its extension-inflation behaviour. The wide range of applications of the constitutive modelling framework to artery walls in both health and disease and to the other fibrous soft tissues is discussed in detail. Since the main modelling effort in the literature has been on the passive response of arteries, this is also the concern of the major part of this article. A section is nevertheless devoted to reviewing the limited literature within the continuum mechanics framework on the active response of artery walls, i.e. the mechanical behaviour associated with the activation of smooth muscle, a very important but also very challenging topic that requires substantial further development. A final section provides a brief summary of the current state of arterial wall mechanical modelling and points to key areas that need further modelling effort in order to improve understanding of the biomechanics and mechanobiology of arteries and other soft tissues, from the molecular, to the cellular, tissue and organ levels.

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Computational model of collagen turnover in carotid arteries during hypertension

Saéz

Peña

Tarbell

et al. 2015

Numer Methods Biomed Eng

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SUMMARYIt is well known that biological tissues adapt their properties due to different mechanical and chemical stimuli. The goal of this work is the study of the collagen turnover in the arterial tissue of hypertensive patients through a coupled computational mechano-chemical model. Although it has been widely studied experimentally, computational models dealing with the mechano-chemical approach are not. The present approach can be extended easily to study other aspects of bone remodeling or collagen degradation in heart diseases. The model can be divided into three different stages. First, we study the smooth muscle cell synthesis of different biological substances due to the over-stretching during hypertension. Next, we study the mass-transport of these substances along the arterial wall. The last step is to compute the turnover of collagen based on the amount of these substances in the arterial wall which interact with each other to modify the turnover rate of collagen. We simulate this process in a finite element model of a real human carotid artery. The final results show the well known stiffening of the arterial wall due to the increase in the collagen content.

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Growth and remodeling in a thick-walled artery model: effects of spatial variations in wall constituents

Cited by 146 publications

References 45 publications

Blast-induced phenotypic switching in cerebral vasospasm

Blast-induced phenotypic switching in cerebral vasospasm

Constitutive modelling of arteries

Computational model of collagen turnover in carotid arteries during hypertension

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