Mechanical Characterization of Vascular Smooth Muscle

Author(s):  
Chantal van den Broek ◽  
Jeroen Nieuwenhuizen ◽  
Marcel Rutten ◽  
Frans van de Vosse

Remodeling of the arterial wall, in response to e.g. induced hypertension, vasoconstriction, and reduced cyclic stretch, has been studied in detail to get insight into vascular pathologies [1]. Constitutive models are helpful to the understanding of the relation between different processes that occur in the arterial wall during remodeling. Including the smooth muscle cell (SMC) behavior in constitutive models is relevant, as those cells may change tone when subjected to an altered mechanical loading and can initiate arterial remodeling.

2014 ◽  
Vol 136 (11) ◽  
Author(s):  
Wilfried Bürzle ◽  
Edoardo Mazza ◽  
John J. Moore

Puncture testing has been applied in several studies for the mechanical characterization of human fetal membrane (FM) tissue, and significant knowledge has been gained from these investigations. When comparing results of mechanical testing (puncture, inflation, and uniaxial tension), we have observed discrepancies in the rupture sequence of FM tissue and significant differences in the deformation behavior. This study was undertaken to clarify these discrepancies. Puncture experiments on FM samples were performed to reproduce previous findings, and numerical simulations were carried out to rationalize particular aspects of membrane failure. The results demonstrate that both rupture sequence and resistance to deformation depend on the samples' fixation. Soft fixation leads to slippage in the clamping, which reduces mechanical loading of the amnion layer and results in chorion rupturing first. Conversely, the stiffer, stronger, and less extensible amnion layer fails first if tight fixation is used. The results provide a novel insight into the interpretation of ex vivo testing as well as in vivo membrane rupture.


2022 ◽  
Vol 119 (3) ◽  
pp. e2117232119
Author(s):  
Giulio Franchini ◽  
Ivan D. Breslavsky ◽  
Francesco Giovanniello ◽  
Ali Kassab ◽  
Gerhard A. Holzapfel ◽  
...  

Experimental data and a suitable material model for human aortas with smooth muscle activation are not available in the literature despite the need for developing advanced grafts; the present study closes this gap. Mechanical characterization of human descending thoracic aortas was performed with and without vascular smooth muscle (VSM) activation. Specimens were taken from 13 heart-beating donors. The aortic segments were cooled in Belzer UW solution during transport and tested within a few hours after explantation. VSM activation was achieved through the use of potassium depolarization and noradrenaline as vasoactive agents. In addition to isometric activation experiments, the quasistatic passive and active stress–strain curves were obtained for circumferential and longitudinal strips of the aortic material. This characterization made it possible to create an original mechanical model of the active aortic material that accurately fits the experimental data. The dynamic mechanical characterization was executed using cyclic strain at different frequencies of physiological interest. An initial prestretch, which corresponded to the physiological conditions, was applied before cyclic loading. Dynamic tests made it possible to identify the differences in the viscoelastic behavior of the passive and active tissue. This work illustrates the importance of VSM activation for the static and dynamic mechanical response of human aortas. Most importantly, this study provides material data and a material model for the development of a future generation of active aortic grafts that mimic natural behavior and help regulate blood pressure.


2001 ◽  
Vol 280 (6) ◽  
pp. H2752-H2760 ◽  
Author(s):  
P. Fridez ◽  
A. Rachev ◽  
J.-J. Meister ◽  
K. Hayashi ◽  
N. Stergiopulos

Recent experimental studies have shown significant alterations of the vascular smooth muscle (VSM) tone when an artery is subjected to an elevation in pressure. Therefore, the VSM participates in the adaptation process not only by means of its synthetic activity (fibronectins and collagen) or proliferative activity (hypertrophy and hyperplasia) but also by adjusting its contractile properties and its tone level. In previous theoretical models describing the time evolution of the arterial wall adaptation in response to induced hypertension, the contribution of VSM tone has been neglected. In this study, we propose a new biomechanical model for the wall adaptation to induced hypertension, including changes in VSM tone. On the basis of Hill's model, total circumferential stress is separated into its passive and active components, the active part being the stress developed by the VSM. Adaptation rate equations describe the geometrical adaptation (wall thickening) and the adaptation of active stress (VSM tone). The evolution curves that are derived from the theoretical model fit well the experimental data describing the adaptation of the rat common carotid subjected to a step increase in pressure. This leads to the identification of the model parameters and time constants by characterizing the rapidity of the adaptation processes. The agreement between the results of this simple theoretical model and the experimental data suggests that the theoretical approach used here may appropriately account for the biomechanics underlying the arterial wall adaptation.


Author(s):  
Arjen van der Horst ◽  
Chantal N. van den Broek ◽  
Marcel C. M. Rutten ◽  
Frans N. van de Vosse

Mechanical characterization of the coronary arterial wall is important for several reasons. Mechanical factors play an important role in the development of atherosclerosis [1]. Atherosclerotic coronary arteries may be treated mechanically with interventions like PTCA and stent implantation, 1265000 PTCA procedures were performed in the United States in 2005 [2]. Furthermore, knowledge of the mechanical properties of the arterial wall is important for modeling of the coronary circulation and explaining its hemodynamics.


2002 ◽  
Vol 283 (6) ◽  
pp. H2714-H2724 ◽  
Author(s):  
Jürgen R. Sindermann ◽  
Philip Babij ◽  
Joseph C. Klink ◽  
Christiane Köbbert ◽  
Gabriele Plenz ◽  
...  

To study the effects of enhanced smooth muscle cell (SMC) proliferation on arterial vessel geometry in the absence of vessel trauma, we developed a transgenic mouse model expressing SV40 large T antigen under control of the 2.3-kb smooth muscle-myosin heavy chain promoter. Transgenic mice studied at ages from 3 to 13 wk showed a 3.2-fold increase in arterial wall SMC density, with 28% of SMC exhibiting proliferative cell nuclear antigen staining, confirming enhanced SMC proliferation, which was accompanied by two- to threefold increases in arterial wall areas ( P < 0.05). Remarkably, despite increased vessel wall mass, the lumen area was not compromised, but rather was increased. A tightly conserved linear relationship was found between arterial circumference and wall thickness with slopes of 0.036 for both transgenics ( r = 0.93, P < 0.01) and controls ( r = 0.77, P < 0.01), suggesting the hypothesis that the conservation of wall stress functions as a primary determinant of adaptive arterial remodeling. This establishes a new model of adaptive vessel remodeling occurring in response to a proliferative input in the absence of mechanical injury or primary flow perturbation.


2004 ◽  
Vol 10 (5-6) ◽  
pp. 699-710 ◽  
Author(s):  
Andrea Remuzzi ◽  
Sara Mantero ◽  
Maurizio Colombo ◽  
Marina Morigi ◽  
Elena Binda ◽  
...  

Author(s):  
Joseph T. Keyes ◽  
Danielle R. Lockwood ◽  
Jonathan P. Vande Geest

The biomechanical characterization of tissue offers insight into items such as progression of disease and design parameters for implants1,2. To biomechanically evaluate the properties of blood vessels, biaxial testing is frequently performed because biological samples often exhibit anisotropy, and are most frequently under tension from the applied pressures and stretches3,4. Deciding whether to splay a tubular sample open to test in planar form versus performing pressure-inflation testing is a decision often determined by what testing equipment is available. The purpose of this abstract is to compare pressure-inflation behavior, stress distributions, and fiber architecture in planar versus tubular biaxial testing of the same arteries.


2007 ◽  
Vol 292 (5) ◽  
pp. H2438-H2448 ◽  
Author(s):  
Stephanie W. Watts ◽  
Catherine Rondelli ◽  
Keshari Thakali ◽  
Xiaopeng Li ◽  
Bruce Uhal ◽  
...  

Arterial remodeling occurs in response to mechanical and neurohumoral stimuli. We hypothesized that veins, which are not exposed to higher pressures in hypertension, would demonstrate less active remodeling than arteries. We assessed remodeling with two standard measures of arterial remodeling: vessel morphometry and the expression/function of matrix metalloproteinases (MMPs). Thoracic aorta and vena cava from sham normotensive and DOCA-salt hypertensive rats (110 ± 4 and 188 ± 8 mmHg systolic blood pressure, respectively) were used. Wall thickness was increased in DOCA-salt vs. sham aorta (301 ± 23 vs. 218 ± 14 μm, P < 0.05), as was medial area, but neither measure was altered in the vena cava. The aorta and vena cava expressed the gelatinases MMP-2, MMP-9, transmembrane proteinase MT1-MMP, and tissue inhibitor of metalloproteinase-2 (TIMP-2). Immunohistochemically, MMP-2 localized to smooth muscle in the aorta and densely in endothelium/smooth muscle of the vena cava. Western and zymographic analyses verified that MMP-2 was active in all vessels and less active in the vena cava than aorta. In hypertension, MMP-2 expression and activity in the aorta were increased (59.1 ± 3.7 and 74.5 ± 6.1 units in sham and DOCA, respectively, P < 0.05); similar elevations were not observed in the vena cava. MMP-9 was weakly expressed in all vessels. MT1-MMP was expressed by the aorta and vena cava and elevated in the vena cava from DOCA-salt rats. TIMP-2 expression was significantly increased in the aorta of DOCA rats compared with sham but was barely detectable in the vena cava of sham or DOCA-salt hypertensive rats. These findings suggest that large veins may not undergo vascular remodeling in DOCA-salt hypertension.


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