Experimental Investigation of the Distribution of Residual Strains in the Artery Wall

1997 ◽  
Vol 119 (4) ◽  
pp. 438-444 ◽  
Author(s):  
S. E. Greenwald ◽  
J. E. Moore ◽  
A. Rachev ◽  
T. P. C. Kane ◽  
J.-J. Meister
Keyword(s):  
Smooth Muscle ◽  
Stress State ◽  
Smooth Muscle Cells ◽  
Residual Strain ◽  
Arterial Wall ◽  
Normal Growth ◽  
Muscle Cells ◽  
Opening Angle ◽  
Artery Wall ◽  
Residual Strains

Arterial wall stresses are thought to be a major determinant of vascular remodeling both during normal growth and throughout the development of occlusive vascular disease. A completely physiologic mechanical model of the arterial wall should account not only for its residual strains but also for its structural nonhomogeneity. It is known that each layer of the artery wall possesses different mechanical properties, but the distribution of residual strain among the different mechanical components, and thus the true zero stress state, remain unknown. In this study, two different sets of experiments were carried out in order to determine the distribution of residual strains in artery walls, and thus the true zero stress state. In the first, collagen and elastin were selectively eliminated by chemical methods and smooth muscle cells were destroyed by freezing. Dissolving elastin provoked a decrease in the opening angle, while dissolving collagen and destroying smooth muscle cells had no effect. In the second, different wall layers of bovine carotid arteries were removed from the exterior or luminal surfaces by lathing or drilling frozen specimens, and then allowing the frozen material to thaw before measuring residual strain. Lathing material away from the outer surface caused the opening angle of the remaining inner layers to increase. Drilling material from the inside caused the opening angle of the remaining outer layers to decrease. Mechanical nonhomogeneity, including the distribution of residual strains, should thus be considered as an important factor in determining the distribution of stress in the artery wall and the configuration of the true zero stress state.

The Contribution of Elastin, Collagen, and Smooth Muscle Cells to Residual Strains in Large Elastic Arteries

2004 ◽  
Author(s):  
Jingli Wang ◽  
Lisa Pruitt
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Strain Gradient ◽  
Residual Strain ◽  
Vessel Wall ◽  
Cell Activation ◽  
Muscle Cells ◽  
Neutral Axis ◽  
Opening Angle ◽  
Residual Strains

The contribution of elastin, collagen, and smooth muscle cells to residual strain in porcine aortas were evaluated by assessing several parameters: opening angle, neutral axis, and residual strain. Elastase or collagenase was used to remove elastin or collagen. Smooth muscle cells were activated using Ca2+/KCl solutions or deactivated using KCN solutions. Several statistically significant trends (P<0.05) were obtained. As elastin was removed, the opening angle increased. As collagen was removed, the opening angle decreased. In addition, the activation of smooth muscle cells reduced the opening angle. Smooth muscle cell activation and collagenase digestion resulted in: 1) a decrease in residual strain and strain gradient, 2) the neutral axis shifting toward the adventitia side of the vessel wall.

Matrix Gla Protein Synthesis and Gamma-carboxylation in the Aortic Vessel Wall and Proliferating Vascular Smooth Muscle Cells

1999 ◽  
Vol 82 (12) ◽  
pp. 1764-1767 ◽  
Author(s):  
Dean Cain ◽  
David Sane ◽  
Reidar Wallin
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vitamin K ◽  
Vessel Wall ◽  
Arterial Wall ◽  
Muscle Cells ◽  
Matrix Gla Protein ◽  
Dt Diaphorase

SummaryMatrix GLA protein (MGP) is an inhibitor of calcification in the arterial wall and its activity is dependent upon vitamin K-dependent γ-carboxylation. This modification is carried out by a warfarin sensitive enzyme system that converts specific Glu residues to γ-carboxyglutamic acid (GLA) residues. Recent studies have demonstrated that the γ-carboxylation system in the arterial wall, in contrast to that in the liver, is unable to use vitamin K as an antidote to warfarin.By use of immunohistochemistry we demonstrate that MGP is expressed in the arterial wall and immunocytochemistry localized the MGP precursors to the endoplasmic reticulum in vascular smooth muscle cells. Resting smooth vascular muscle cells in the aortic wall and proliferating cells from explants of the aorta have all the enzymes needed for γ-carboxylation of MGP. However, when compared to the liver system, expression of the enzymes of the γ-carboxylation system in vascular smooth muscle cells is different. Of particular interest is the finding that the specific activity of the warfarin sensitive enzyme vitamin K epoxide reductase is 3-fold higher in vascular smooth muscle cells than in liver. DT-diaphorase, which catalyses the antidotal pathway for vitamin K reduction in liver, is 100-fold less active in resting vascular smooth muscle cells than in liver. Data obtained from an in vitro γ-carboxylation system suggest that the antidotal pathway catalyzed by DT-diaphorase in the vessel wall is unable to provide the carboxylase with enough reduced vitamin K to trigger γ-carboxylation of MGP. This finding provides an explanation to the inability of vitamin K to work as an antidote to warfarin intoxication of the arterial wall. Therefore the vitamin K dependent γ-carboxylation system in the arterial wall share a common feature with the system in bone cells by being unable to utilize vitamin K as an antidote.

Distribution of shear stress over smooth muscle cells in deformable arterial wall

2008 ◽  
Vol 46 (7) ◽  
pp. 649-657 ◽  
Author(s):  
Mahsa Dabagh ◽  
Payman Jalali ◽  
Yrjö T. Konttinen ◽  
Pertti Sarkomaa
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Muscle Cells

Computational study on phase lag of arterial-wall motion for assessment of plaque vulnerability

2020 ◽  
Vol 234 (5) ◽  
pp. 517-526
Author(s):  
Pengsrorn Chhai ◽  
Kyehan Rhee
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Wall Motion ◽  
Arterial Wall ◽  
Computational Study ◽  
Muscle Cells ◽  
Phase Lag ◽  
Plaque Vulnerability ◽  
Wall Displacement ◽  
Lipid Core

The wall motion of atherosclerotic plaque was analyzed using a computational method, and the effects of tissue viscoelasticity, fibrosis thickness, and lipid-core stiffness on wall displacement waveforms were examined. The viscoelasticity of plaque tissues was modeled using a time Prony series with four Maxwell elements. Computational simulation of tissue indentation tests showed the validity of the proposed viscoelastic constitutive models. Decreasing the relative moduli of the viscoelastic model reduced their viscous characteristics while enhancing the stiffness of the wall, which corresponded with the effects of decreased smooth muscle cells content. A finite-element analysis was conducted for atherosclerotic wall models and wall displacement waveforms were computed. The phase difference between the first harmonics of pressure and displacement waves was selected to represent the time delay of the wall motion. As the relative modulus decreased, the wall displacement and phase lag decreased. A thinner wall and softer lipid core corresponded to a greater wall displacement and smaller phase lag. Because the phase lag of the arterial-wall motion was smaller for the plaque with a thinner cap, lower smooth muscle cells content, and softer lipid core (all features of plaques with high rupture risk), first harmonics of pressure and displacement waves can be used as an index to assess plaque vulnerability.

Smooth Muscle Cells Influence Monocyte Response to LDL as well as Their Adhesion and Transmigration in a Coculture Model of the Arterial Wall

2001 ◽  
Vol 38 (5) ◽  
pp. 479-491 ◽  
Author(s):  
Fabienne Kinard ◽  
Kathy Jaworski ◽  
Thérèse Sergent-Engelen ◽  
Dan Goldstein ◽  
Paul P. van Veldhoven ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Muscle Cells ◽  
Coculture Model

Calcium sensitivity of vasospastic basilar artery after experimental subarachnoid hemorrhage

2006 ◽  
Vol 290 (6) ◽  
pp. H2329-H2336 ◽  
Author(s):  
R. Loch Macdonald ◽  
Zhen-Du Zhang ◽  
Masataka Takahashi ◽  
Elena Nikitina ◽  
J. Young ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Arterial Compliance ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Calcium Sensitivity ◽  
Basilar Arteries

Arteries that develop vasospasm after subarachnoid hemorrhage (SAH) may have altered contractility and compliance. Whether these changes are due to alterations in the smooth muscle cells or the arterial wall extracellular matrix is unknown. This study elucidated the location of such changes and determined the calcium sensitivity of vasospastic arteries. Dogs were placed under general anesthesia and underwent creation of SAH using the double-hemorrhage model. Vasospasm was assessed by angiography performed before and 4, 7, or 21 days after SAH. Basilar arteries were excised from SAH or control dogs ( n = 8–52 arterial rings from 2–9 dogs per measurement) and studied under isometric tension in vitro before and after permeabilization of smooth muscle with α-toxin. Endothelium was removed from all arteries. Vasospastic arteries demonstrated significantly reduced contractility to KCl with a shift in the EC50 toward reduced sensitivity to KCl 4 and 7 days after SAH ( P < 0.05, ANOVA). There was reduced compliance that persisted after permeabilization ( P < 0.05, ANOVA). Calcium sensitivity was decreased during vasospasm 4 and 7 days after SAH, as assessed in permeabilized arteries and in those contracted with BAY K 8644 in the presence of different concentrations of extracellular calcium ( P < 0.05, ANOVA). Depolymerization of actin with cytochalasin D abolished contractions to KCl but failed to alter arterial compliance. In conclusion, it is shown for the first time that calcium sensitivity is decreased during vasospasm after SAH in dogs, suggesting that other mechanisms are involved in maintaining the contraction. Reduced compliance seems to be due to an alteration in the arterial wall extracellullar matrix rather than the smooth muscle cells themselves because it cannot be alleviated by depolymerization of smooth muscle actin.

scholarly journals MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells

2005 ◽  
Vol 202 (5) ◽  
pp. 663-671 ◽  
Author(s):  
Sergey Filippov ◽  
Gerald C. Koenig ◽  
Tae-Hwa Chun ◽  
Kevin B. Hotary ◽  
Ichiro Ota ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Matrix Metalloproteinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Arterial Wall ◽  
Neointimal Hyperplasia ◽  
Muscle Cells

During pathologic vessel remodeling, vascular smooth muscle cells (VSMCs) embedded within the collagen-rich matrix of the artery wall mobilize uncharacterized proteolytic systems to infiltrate the subendothelial space and generate neointimal lesions. Although the VSMC-derived serine proteinases, plasminogen activator and plasminogen, the cysteine proteinases, cathepsins L, S, and K, and the matrix metalloproteinases MMP-2 and MMP-9 have each been linked to pathologic matrix-remodeling states in vitro and in vivo, the role that these or other proteinases play in allowing VSMCs to negotiate the three-dimensional (3-D) cross-linked extracellular matrix of the arterial wall remains undefined. Herein, we demonstrate that VSMCs proteolytically remodel and invade collagenous barriers independently of plasmin, cathepsins L, S, or K, MMP-2, or MMP-9. Instead, we identify the membrane-anchored matrix metalloproteinase, MT1-MMP, as the key pericellular collagenolysin that controls the ability of VSMCs to degrade and infiltrate 3-D barriers of interstitial collagen, including the arterial wall. Furthermore, genetic deletion of the proteinase affords mice with a protected status against neointimal hyperplasia and lumen narrowing in vivo. These studies suggest that therapeutic interventions designed to target MT1-MMP could prove beneficial in a range of human vascular disease states associated with the destructive remodeling of the vessel wall extracellular matrix.

scholarly journals Factors Controlling Growth of Arterial Cells following Injury*

1990 ◽  
Vol 18 (4a) ◽  
pp. 547-553 ◽  
Author(s):  
Michael A. Reidy ◽  
Christopher L. Jackson
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Arterial Wall ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Experimental Models ◽  
Smooth Muscle Cell Proliferation

The proliferation of vascular smooth muscle cells is a key event in the development of arterial lesions. In experimental models, loss of arterial endothelium followed by platelet adherence does not necessarily stimulate smooth muscle cell proliferation. Furthermore, using animals deficient in platelets, smooth muscle cell proliferation was induced to an equal extent as in control animals following injury with a balloon catheter. Modulation of the smooth muscle response, however, was achieved by totally denuding arteries with a technique which did not traumatize medial cells. These data suggested that injury and cell death might induce proliferation of cells by release of endogenous mitogen. Basic FGF is present in the arterial wall and addition of this mitogen to denuded arteries was found to cause a highly significant increase in smooth muscle cell proliferation. These studies suggest that smooth muscle cell proliferation could be induced by factors present in the arterial wall and does not require exogenous factors. Smooth muscle cell proliferation following balloon catheter injury is significantly reduced by administration of calcium antagonists. Repeated administration of nifedipine caused a significant reduction in intimal lesion size induced by injury. The anti-proliferative. effect was not observed in other tissues. Influx of Ca++ ions into medial smooth muscle cells may therefore be an obligatory step for replication.

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