Relevant bibliographies by topics / Arteries – Elastic properties

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Arteries – Elastic properties'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Arteries – Elastic properties"

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Cocciolone, Austin J., Jie Z. Hawes, Marius C. Staiculescu, Elizabeth O. Johnson, Monzur Murshed, and Jessica E. Wagenseil. "Elastin, arterial mechanics, and cardiovascular disease." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (August 1, 2018): H189—H205. http://dx.doi.org/10.1152/ajpheart.00087.2018.

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Large, elastic arteries are composed of cells and a specialized extracellular matrix that provides reversible elasticity and strength. Elastin is the matrix protein responsible for this reversible elasticity that reduces the workload on the heart and dampens pulsatile flow in distal arteries. Here, we summarize the elastin protein biochemistry, self-association behavior, cross-linking process, and multistep elastic fiber assembly that provide large arteries with their unique mechanical properties. We present measures of passive arterial mechanics that depend on elastic fiber amounts and integrity such as the Windkessel effect, structural and material stiffness, and energy storage. We discuss supravalvular aortic stenosis and autosomal dominant cutis laxa-1, which are genetic disorders caused by mutations in the elastin gene. We present mouse models of supravalvular aortic stenosis, autosomal dominant cutis laxa-1, and graded elastin amounts that have been invaluable for understanding the role of elastin in arterial mechanics and cardiovascular disease. We summarize acquired diseases associated with elastic fiber defects, including hypertension and arterial stiffness, diabetes, obesity, atherosclerosis, calcification, and aneurysms and dissections. We mention animal models that have helped delineate the role of elastic fiber defects in these acquired diseases. We briefly summarize challenges and recent advances in generating functional elastic fibers in tissue-engineered arteries. We conclude with suggestions for future research and opportunities for therapeutic intervention in genetic and acquired elastinopathies.
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Fonck, E., G. Prod'hom, S. Roy, L. Augsburger, D. A. Rüfenacht, and N. Stergiopulos. "Effect of elastin degradation on carotid wall mechanics as assessed by a constituent-based biomechanical model." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (June 2007): H2754—H2763. http://dx.doi.org/10.1152/ajpheart.01108.2006.

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Arteries display a nonlinear anisotropic behavior dictated by the elastic properties and structural arrangement of its main constituents, elastin, collagen, and vascular smooth muscle. Elastin provides for structural integrity and for the compliance of the vessel at low pressure, whereas collagen gives the tensile resistance required at high pressures. Based on the model of Zulliger et al. (Zulliger MA, Rachev A, Stergiopulos N. Am J Physiol Heart Circ Physiol 287: H1335–H1343, 2004), which considers the contributions of elastin, collagen, and vascular smooth muscle cells (VSM) in an explicit form, we assessed the effects of enzymatic degradation of elastin on biomechanical properties of rabbit carotids. Pressure-diameter curves were obtained for controls and after elastin degradation, from which elastic and structural properties were derived. Data were fitted into the model of Zulliger et al. to assess elastic constants of elastin and collagen as well as the characteristics of the collagen engagement profile. The arterial segments were also prepared for histology to visualize and quantify elastin and collagen. Elastase treatment leads to a diameter enlargement, suggesting the existence of significant compressive prestresses within the wall. The elastic modulus was more ductile in treated arteries at low circumferential stretches and significantly greater at elevated circumferential stretches. Abrupt collagen fiber recruitment in elastase-treated arteries leads to a much stiffer vessel at high extensions. This change in collagen engagement properties results from structural alterations provoked by the degradation of elastin, suggesting a clear interaction between elastin and collagen, often neglected in previous constituent-based models of the arterial wall.
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Stephanis, C. G., D. E. Mourmouras, and D. G. Tsagadopoulos. "On the elastic properties of arteries." Journal of Biomechanics 36, no. 11 (November 2003): 1727–31. http://dx.doi.org/10.1016/s0021-9290(03)00188-x.

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Laurant, Pascal, Mark Adrian, and Alain Berthelot. "Effect of age on mechanical properties of rat mesenteric small arteries." Canadian Journal of Physiology and Pharmacology 82, no. 4 (April 1, 2004): 269–75. http://dx.doi.org/10.1139/y04-026.

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With aging, large arteries become stiffer and systolic blood pressure consequently increases. Less is known, however, about the age-related change in mechanics of small resistance arteries. The aim of this study was to determine whether aging plays a role in the stiffening of the small mesenteric arteries of rats. Intra-arterial systolic, diastolic, mean and pulse pressures were measured in male Wistar rats aged 2, 4, 15 and 26 months. The passive mechanical properties of the wall of isolated perfused and pressurized arterial segments of mesenteric small arteries were also investigated. Intra-arterial systolic, diastolic and mean blood pressures tended to decrease with age and were significantly lower in the oldest rats (26-month-old group). Pulse pressure was significantly higher in the 15- and 26-month-old groups than in the two younger groups. Under isobaric conditions, increasing age is associated with an outward hypertrophic remodeling of the mesenteric arteries. Under relaxed conditions, incremental distensibility in response to increasing intravascular pressure did not change with aging. As a function of strain (under isometric conditions), stress shifted to the left as age increased, indicating an age-related vascular stiffening. Under isobaric conditions or in relation to wall stress, the elastic modulus was greater in the adult 15-month-old rats than in the younger rats. These findings suggest that distensibility seems to be preserved with aging, despite stiffness of the wall components, probably by arterial wall geometric adaptation, which limits the pulse pressure damage. It is interesting to note that elastic modulus in mesenteric arteries from the oldest rats (26-month-old), examined in relation to wall stress and intravascular pressure, did not differ from that of the youngest rats, thus suggesting that elasticity of wall components had been restored.Key words: age, arteries, elastic modulus, stiffness, pressure.
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Bank, Alan J. "Physiologic Aspects of Drug Therapy and Large Artery Elastic Properties." Vascular Medicine 2, no. 1 (February 1997): 44–50. http://dx.doi.org/10.1177/1358863x9700200107.

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Vasoactive drugs alter smooth muscle tone not only in arterial resistance vessels, but also in large conduit arteries. The resultant changes in smooth muscle tone alter both conduit vessel size and stiffness and hence influence pulsatile components of left ventricular afterload. The effects of smooth muscle relaxation and contraction on arterial elastic properties are complex and have not been fully characterized. Several recent studies have utilized a new intravascular ultrasound technique to study the effects of changes in smooth muscle tone on brachial artery elastic mechanics in normal human subjects in vivo. Smooth muscle relaxation with nitroglycerin improves isobaric brachial artery compliance without significantly altering arterial wall stiffness as measured by incremental elastic modulus ( Einc). The improvement in compliance with smooth muscle relaxation is the net result of factors that: (1) increase wall stiffness (increased tension in parallel elastin and collagen fibers); (2) decrease wall stiffness (decreased tension in the smooth muscle and its associated series elastic component); and (3) increase vessel lumen size. Using a modified Maxwell model for the arterial wall, smooth muscle relaxation is also shown to shift the predominant elements contributing to wall stress and EInc from smooth muscle and the collagen fibers in series with the smooth muscle to collagen fibers in parallel with the smooth muscle. A better understanding of the mechanisms contributing to changes in arterial elastic mechanics following alterations in smooth muscle tone will help in developing pharmacologic therapies aimed at reducing pulsatile components of left ventricular afterload.
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Guo, X., M. J. Oldham, M. T. Kleinman, R. F. Phalen, and G. S. Kassab. "Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 5 (November 2006): H2354—H2361. http://dx.doi.org/10.1152/ajpheart.00376.2006.

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Cigarette smoking (CS) is a major risk factor for vascular disease. The aim of this study was to quantitatively assess the influence of CS on mouse arteries. We studied the effect of short-term (6 wk) and long-term (16 wk) CS exposure on structural and mechanical properties of coronary arteries compared with that of control mice. We also examined the reversibility of the deleterious effects of CS on structural [e.g., wall thickness (WT)], mechanical (e.g., stiffness), and biochemical [e.g., nitric oxide (NO) by-products] properties with the cessation of CS. The left and right coronary arteries were cannulated in situ and mechanically distended. The stress, strain, elastic modulus, and WT of coronary arteries were determined. Western blot analysis was used to analyze endothelial NO synthase (eNOS) in the femoral and carotid arteries of the same mice, and NO by-products were determined by measuring the levels of nitrite. Our results show that the mean arterial pressure was increased by CS. Furthermore, CS significantly increased the elastic modulus, decreased stress and strain, and increased the WT and WT-to-radius ratio compared with those of control mice. The reduction of eNOS protein expression was found only after long-term CS exposure. Moreover, the NO metabolite was markedly decreased in CS mice after short- and long-term exposure of CS. These findings suggest that 16 wk of CS exposure can cause an irreversible deterioration of structural and elastic properties of mouse coronary arteries. The decrease in endothelium-derived NO in CS mice was seen to significantly correlate with the remodeling of arterial wall.
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Su, Junjing, Charmilie C. Logan, Alun D. Hughes, Kim H. Parker, Niti M. Dhutia, Carl Christian Danielsen, and Ulf Simonsen. "Impact of chronic hypoxia on proximal pulmonary artery wave propagation and mechanical properties in rats." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 6 (June 1, 2018): H1264—H1278. http://dx.doi.org/10.1152/ajpheart.00695.2017.

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Arterial stiffness and wave reflection are important components of the ventricular afterload. Therefore, we aimed to assess the arterial wave characteristics and mechanical properties of the proximal pulmonary arteries (PAs) in the hypoxic pulmonary hypertensive rat model. After 21 days in normoxic or hypoxic chambers (24 animals/group), animals underwent transthoracic echocardiography and PA catheterization with a dual-tipped pressure and Doppler flow sensor wire. Wave intensity analysis was performed. Artery rings obtained from the pulmonary trunk, right and left PAs, and aorta were subjected to a tensile test to rupture. Collagen and elastin content were determined. In hypoxic rats, proximal PA wall thickness, collagen content, tensile strength per unit collagen, maximal elastic modulus, and wall viscosity increased, whereas the elastin-to-collagen ratio and arterial distensibility decreased. Arterial pulse wave velocity was also increased, and the increase was more prominent in vivo than ex vivo. Wave intensity was similar in hypoxic and normoxic animals with negligible wave reflection. In contrast, the aortic maximal elastic modulus remained unchanged, whereas wall viscosity decreased. In conclusion, there was no evidence of altered arterial wave propagation in proximal PAs of hypoxic rats while the extracellular matrix protein composition was altered and collagen tensile strength increased. This was accompanied by altered mechanical properties in vivo and ex vivo. NEW & NOTEWORTHY In rats exposed to chronic hypoxia, we have shown that pulse wave velocity in the proximal pulmonary arteries increased and pressure dependence of the pulse wave velocity was steeper in vivo than ex vivo leading to a more prominent increase in vivo.
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Arribas, Silvia M., Ana M. Briones, Catherine Bellingham, M. Carmen González, Mercedes Salaices, Kela Liu, Yanting Wang, and Aleksander Hinek. "Heightened aberrant deposition of hard-wearing elastin in conduit arteries of prehypertensive SHR is associated with increased stiffness and inward remodeling." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 6 (December 2008): H2299—H2307. http://dx.doi.org/10.1152/ajpheart.00155.2008.

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Elastin is a major component of conduit arteries and a key determinant of vascular viscoelastic properties. Aberrant organization of elastic lamellae has been reported in resistance vessels from spontaneously hypertensive rats (SHR) before the development of hypertension. Hence, we have characterized the content and organization of elastic lamellae in conduit vessels of neonatal SHR in detail, comparing the carotid arteries from 1-wk-old SHR with those from Wistar-Kyoto (WKY) and Sprague Dawley (SD) rats. The general structure and mechanics were studied by pressure myography, and the internal elastic lamina organization was determined by confocal microscopy. Cyanide bromide-insoluble elastin scaffolds were also prepared from 1-mo-old SHR and WKY aortas to assess their weight, amino acid composition, three-dimensional lamellar organization, and mechanical characteristics. Carotid arteries from 1-wk-old SHR exhibited narrower lumen and greater intrinsic stiffness than those from their WKY and SD counterparts. These aberrations were associated with heightened elastin content and with a striking reduction in the size of the fenestrae present in the elastic lamellae. The elastin scaffolds isolated from SHR aortas also exhibited increased relative weight and stiffness, as well as the presence of peculiar trabeculae inside the fenestra that reduced their size. We suggest that the excessive and aberrant elastin deposited in SHR vessels during perinatal development alters their mechanical properties. Such abnormalities are likely to compromise vessel expansion during a critical period of growth and, at later stages, they could compromise hemodynamic function and participate in the development of systemic hypertension.
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Lammers, Steven R., Phil H. Kao, H. Jerry Qi, Kendall Hunter, Craig Lanning, Joseph Albietz, Stephen Hofmeister, Robert Mecham, Kurt R. Stenmark, and Robin Shandas. "Changes in the structure-function relationship of elastin and its impact on the proximal pulmonary arterial mechanics of hypertensive calves." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1451—H1459. http://dx.doi.org/10.1152/ajpheart.00127.2008.

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Extracellular matrix remodeling has been proposed as one mechanism by which proximal pulmonary arteries stiffen during pulmonary arterial hypertension (PAH). Although some attention has been paid to the role of collagen and metallomatrix proteins in affecting vascular stiffness, much less work has been performed on changes in elastin structure-function relationships in PAH. Such work is warranted, given the importance of elastin as the structural protein primarily responsible for the passive elastic behavior of these conduit arteries. Here, we study structure-function relationships of fresh arterial tissue and purified arterial elastin from the main, left, and right pulmonary artery branches of normotensive and hypoxia-induced pulmonary hypertensive neonatal calves. PAH resulted in an average 81 and 72% increase in stiffness of fresh and digested tissue, respectively. Increase in stiffness appears most attributable to elevated elastic modulus, which increased 46 and 65%, respectively, for fresh and digested tissue. Comparison between fresh and digested tissues shows that, at 35% strain, a minimum of 48% of the arterial load is carried by elastin, and a minimum of 43% of the change in stiffness of arterial tissue is due to the change in elastin stiffness. Analysis of the stress-strain behavior revealed that PAH causes an increase in the strains associated with the physiological pressure range but had no effect on the strain of transition from elastin-dominant to collagen-dominant behavior. These results indicate that mechanobiological adaptations of the continuum and geometric properties of elastin, in response to PAH, significantly elevate the circumferential stiffness of proximal pulmonary arterial tissue.
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Mackey, K., M. C. Meyer, W. S. Stirewalt, B. C. Starcher, and M. K. McLaughlin. "Composition and mechanics of mesenteric resistance arteries from pregnant rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 1 (July 1, 1992): R2—R8. http://dx.doi.org/10.1152/ajpregu.1992.263.1.r2.

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We tested the hypothesis that the systemic resistance vasculature of the rat is remodeled during pregnancy as evidenced by significant alterations in the passive mechanical properties and extracellular matrix proteins in mesenteric arteries. Mechanical characteristics were determined for arteries from 20-day pregnant rats (n = 6) and age-matched controls (n = 5). Lumen diameter and wall thickness were measured in pressurized arteries (250-microns diameter) using a dimension analyzing system. Distensibility (the relative change in diameter per unit change in pressure) was less in the arteries from the pregnant rats (P less than 0.01). The calculated stress-strain relationships and elastic moduli indicated that the arteries were less stiff by late gestation (P less than 0.05). Ultramicro amino acid analysis and radioimmunoassay were used to measure hydroxyproline, desmosine, and leucine as indicators of collagen, elastin, and total protein, respectively, in similar-sized arteries. Hydroxyproline/leucine (index of collagen) and desmosine/leucine (elastin concentration) decreased 19 and 15% by late gestation (P less than 0.05). The significant alterations in passive mechanics and in extracellular protein content support the concept that arterial wall remodeling in the peripheral vasculature may be one component of the cardiovascular adaptations during pregnancy.
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Dissertations / Theses on the topic "Arteries – Elastic properties"

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Hillery, Claire. "The role of elastin in the mechanical properties of conduit arteries." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417835.

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Goudot, Guillaume. "Applications innovantes des ultrasons en pathologie vasculaire : utilisation de l'imagerie ultrarapide dans l'analyse de la rigidité artérielle et des ultrasons pulsés en thérapie Arterial stiffening assessed by ultrafast ultrasound imaging gives new insight into arterial phenotype of vascular Ehlers–Danlos mouse models Aortic wall elastic properties in case of bicuspid aortic valve Segmental aortic stiffness in bicuspid aortic valve patients compared to first-degree relatives Wall shear stress measurement by ultrafast vector flow imaging for atherosclerotic carotid stenosis Pulsed cavitational therapy using high-frequency ultrasound for the treatment of deep vein thrombosis in an in vitro model of human blood clot." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2215&f=13951.

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Books on the topic "Arteries – Elastic properties"

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Hasegawa, Hideyuki. Ultrasonic methods for measurement of small motion and deformation of biological tissues for assessment of viscoelasticity. New York, NY, USA: ASME, 2014.

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Kanai, Hiroshi, and Hideyuki Hasegawa. Ultrasonic Methods for Measurement of Small Motion and Deformation of Biological Tissues for Assessment of Viscoelasticity. Momentum Press, 2014.

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Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.

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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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Book chapters on the topic "Arteries – Elastic properties"

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Taylor, M. G. "The Optimum Elastic Properties of Arteries." In Ciba Foundation Symposium - Circulatory and Respiratory Mass Transport, 136–52. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719671.ch9.

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Pandian, Natesa G., Tsui-Lieu Hsu, and Andrew Weintraub. "Potential of Intravascular Ultrasound Imaging in the Evaluation of Morphology, Elastic Properties and Vasomotor Function of Coronary Arteries." In Restenosis after Intervention with New Mechanical Devices, 63–71. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2650-2_4.

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Aznaouridis, Konstantinos, Saurabh S. Dhawan, and Arshed A. Quyyumi. "Cardiovascular Risk Prediction by Measurement of Arterial Elastic Properties and Wall Thickness." In Advances in Vascular Medicine, 399–421. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-637-3_22.

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Yamakoshi, Ken-ichi, and Akira Kamiya. "Noninvasive measurement of arterial blood pressure and elastic properties using photoelectric plethysmography technique." In Medical Progress through Technology, 123–43. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3361-3_12.

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Rodriguez-Pascual, Fernando. "The Evolutionary Origin of Elastin: Is Fibrillin the Lost Ancestor?" In Extracellular Matrix - Developments and Therapeutics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95411.

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Elastin is the extracellular matrix protein providing large arteries, lung parenchyma and skin with the properties of extensibility and elastic recoil. Within these tissues, elastin is found as a polymer formed by tropoelastin monomers assembled and cross-linked. In addition to specific protein regions supporting the covalent cross-links, tropoelastin is featured by the presence of highly repetitive sequences rich in proline and glycine making up the so-called hydrophobic domains. These protein segments promote structural flexibility and disordered protein properties, a fundamental aspect to explain its elastomeric behavior. Unlike other matrix proteins such as collagens or laminins, elastin emerged relatively late in evolution, appearing at the divergence of jawed and jawless fishes, therefore present in all species from sharks to humans, but absent in lampreys and other lower chordates and invertebrates. In spite of an intense interrogation of the key aspects in the evolution of elastin, its origin remains still elusive and an ancestral protein that could give rise to a primordial elastin is not known. In this chapter, I review the main molecular features of tropoelastin and the available knowledge on its evolutionary history as well as establish hypotheses for its origin. Considering the remarkable similarities between the hydrophobic domains of the first recognizable elastin gene from the elasmobranch Callorhinchus milii with certain fibrillin regions from related fish species, I raise the possibility that fibrillins might have provided protein domains to an ancestral elastin that thereafter underwent significant evolutionary changes to give the elastin forms found today.
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Erbel, Raimund. "The normal aorta." In ESC CardioMed, edited by Raimund Erbel, 2567–70. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0606.

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The aorta connects the left ventricle to the limb arteries. The segmentation includes different landmarks of the thoracic and abdominal aorta used to describe the integrity of the whole aorta. The aorta can be regarded as a connecting tube with elastic properties for pulsatile continuous flow with systolic forward and early diastolic backward flow in the ascending aorta. Different techniques have been used for measurement of elastic aortic properties, for example, pulse wave velocity correlates with cardiovascular risk and can regarded as a surrogate parameter for risk prediction. It received a class IIa, level of evidence B recommendation in the 2014 European Society of Cardiology Guidelines on the diagnosis and treatment of aortic diseases. Normal values of the aorta have been presented for men and women and demonstrate a continuous enlargement during ageing. Aortic diameters depend on body mass index and age, increasing by approximately 0.9 mm in men and 0.7 mm in women for each decade of life. For clinical use, the diameter indexes have not been found to be of additional value except for people with stature abnormalities. In the future, not only diameters but also parameters of aortic distensibility, elasticity, and flow patterns will be used in order to better identify patients at risk.
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Erman, Burak, and James E. Mark. "Bioelastomers." In Structures and Properties of Rubberlike Networks. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195082371.003.0017.

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There are a variety of biopolymeric materials which exhibit rubberlike elasticity. This is perhaps to be expected when one recalls that most biopolymers are randomly coiled chains with considerable flexibility, and that they are frequently covalently cross-linked or have sufficient numbers of aggregated units to exist in network structures. One very large group of plant materials, the polysaccharides, are in this category, and they do require some elastomeric properties in their functioning. In many of these cases, however, the cross-linking is there primarily for a secondary purpose, such as preventing solubility. When swollen with water or aqueous solutions, such polysaccharides form gels which do exhibit the high deformability and recoverability that are the hallmarks of rubberlike elasticity. Not surprisingly, however, relatively few mechanical property measurements have been carried out to characterize the structures of these gels. The bioelastomers occurring in animals, including vertebrates and mammals, however, are there specifically for their rubberlike elasticity. They are vital, for example, for the functioning of skin, arteries and veins, and much of the lung and heart tissue. Since they are produced by the ribosome “factories” in the body, they are proteins. Thus, the major focus of this chapter is on those proteins specifically designed to function as bioelastomers. It is useful to summarize some general information on bioelastomers that is presented elsewhere. Even with the temporary restriction to bioelastomers which are proteins, there is an almost staggering variety of interesting materials. For example, there is elastin in vertebrates (including mammals) resilin in insects abductin in mollusks, arterial elastomer in octopuses, circulatory and locomotional proteins in cephalopods, and viscid silk in spider webs. Since they are mammals, polymer scientists and engineers who are interested in bioelastomers have focused heavily on elastin! Any materials of this type, however, are worth studying in their own right, to learn more about rubberlike elasticity and biological function. Such studies should also provide guidance on how Nature might be mimicked by synthetic chemists, to produce better nonbiological elastomers.
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Conference papers on the topic "Arteries – Elastic properties"

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Valdez-Jasso, Daniela, Mansoor A. Haider, Stephen L. Campbell, Daniel Bia, Yanina Zocalo, Ricardo L. Armentano, and Mette S. Olufsen. "Modeling Viscoelastic Wall Properties of Ovine Arteries." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205640.

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Generation of a complete map of arterial wall mechanical properties can improve treatment of cardiovascular diseases via contributions to design of patient specific vascular substitutes used to alleviate atherosclerosis and stenoses, which are predominant in arterial pathways (i.e., abdominal aorta, carotids, or femoral arteries). Clinically useful estimation of arterial properties from patient data requires both efficient algorithms and models that are both complex enough to capture clinically important properties and simple enough to allow rapid computation. In this study, we used mechanical models accounting for both elastic and viscoelastic wall deformation to analyze how vessel properties and associated model parameters vary with artery type. It is known that for the aorta wall, deformation is dominated by nonlinear elastic dynamics, while for the smaller vessels (e.g. the carotid artery) deformation is dominated by viscoelastic responses. The latter is correlated with composition of the vessels; the aorta contains significantly less smooth muscle cells (∼40%) than the carotid artery (∼60%), and has significantly more elastin (see Fig 1).
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Chow, Ming-Jay, Raphaël Turcotte, and Katherine Yanhang Zhang. "Elastin in the Arterial ECM: Interactions With Collagen and the Mechanical Properties After Elastin Degradation." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14257.

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Elastin and collagen are the main structural components in the extracellular matrix (ECM) that contribute to the anisotropic and hyperelastic passive mechanical behavior of elastic arteries. It is commonly accepted that the elastin fibers support most of the load at the onset of stretching while collagen fiber recruitment and the transition to collagen bearing the load occurs at higher pressures [1]. Various diseases lead to changes in the ECM, for example in aortic aneurysm there is reduced elastin, excess aged collagen, and fragmentation of the elastic lamellae [2]. Likewise hypertension has been shown to increase arterial collagen and wall thickness with increased stiffness [3]. Improving our knowledge of how the ECM structure affects the mechanical behavior of arteries can provide insights to disease progression and better treatment methods.
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Kao, Philip, H. Jerry Qi, Steve Lammers, and Robin Shandas. "A Comparative Study of Mechanical Properties of Fresh and Elastic-Network Only Proximal Artery Tissues." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176546.

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The contribution of the elastic network to the mechanical behavior of arterial tissues is not well quantified. This paper focuses on the quantification of the behavior of fresh and elastic-network-only (digested) calf arterial tissues in uniaxial deformation using the anisotropic hyperelastic model proposed by Bischoff et al. ([1]). This model characterizes an orthotropic, hyperelastic response, which is well-suited for the modeling of arterial tissues ([2],[3]). For this paper, we attempt to match the material constants associated with the Bischoff-Arruda anisotropic hyperelastic model to our experimental data from arterial tissues including the ascending aortic arch, descending aorta, main, left, and right pulmonary arteries, using a least-squares method. The material parameters obtained from the data fit provide a quantitative comparison of mechanical properties of fresh artery tissues and elastin networks.
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Li, Ye, and Ashraf W. Khir. "Measurements of Wave Speed and Distensibility in Elastic Tubes Using the Diameter-Velocity Loop." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206475.

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The mechanical properties of arterial walls play an important role in the regulation of cardiovascular hemodynamics. In the past decades, arterial wall dynamics attracted much attention and several methods have been proposed to assess the mechanical properties of the human arteries [1].
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Taviani, Valentina, Zhi-Yong Li, Victoria Young, Michael P. F. Sutcliffe, Pauline Wong, Martin J. Graves, and Jonathan H. Gillard. "In Vivo MRI-Based Estimation of Time-Dependent Elastic Modulus in Healthy Arteries." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193000.

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The elastic properties of the arterial wall have been the subject of physiological, clinical and biomedical research for many years. There is convincing evidence that the elastic properties of the large arteries are seriously impaired in the presence of cardiovascular disease (CVD), due to alterations in the intrinsic structural and functional characteristics of vessels [1]. Early detection of changes in the elastic modulus of arteries would provide a powerful tool for both monitoring patients at high cardiovascular risk and testing the effects of pharmaceuticals aimed at stabilizing existing plaques by stiffening them or lowering the lipids.
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Espinosa, Gabriela, Lisa Bennett, William Gardner, and Jessica Wagenseil. "The Effects of Extracellular Matrix Protein Insufficiency and Treatment on the Stiffness of Arterial Smooth Muscle Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14131.

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Increased arterial stiffness is directly correlated with hypertension and cardiovascular disease. Stiffness of the conducting arteries is largely determined by the extracellular matrix (ECM) proteins in the wall, such as collagen and elastin, produced by the smooth muscle cells (SMCs) found in the medial layer. Elastin is deposited as soluble tropoelastin and is later crosslinked into elastin fibers. Newborn mice lacking the elastin protein ( Eln−/−) have increased arterial wall stiffness and SMCs with altered proliferation, migration and morphology [1]. Vessel elasticity is also mediated by other ECM proteins, such as fibulin-4. Elastic tissue, such as lung, skin, and arteries, from fibulin-4 deficient ( Fbln4−/−) mice show no decrease in elastin content, but have reduced elasticity due to disrupted elastin fibers [2]. Arteries from both elastin and fibulin-4 deficient mice have been previously studied, but the mechanical properties of their SMCs have not been investigated. Recent experiments comparing arterial SMCs from old and young animals suggest that mechanical properties of the SMCs themselves may contribute to changes in wall stiffness [3]. Hence, we investigated the stiffness of isolated arterial SMCs from elastin and fibulin-4 deficient mice using atomic force microscopy (AFM). In addition, we studied the effects of two elastin treatments on the mechanical properties of SMCs from Eln+/+ and Eln−/− mice. Differences between the treatments may elucidate the importance of soluble versus crosslinked elastin on single cell stiffness.
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Mogharrabi, Farshad, Jonathan Kuhlenhoelter, Blake Anderson, Katalin Kauser, and Kenneth Monson. "Effect of Photoactivated Cross-Linking Compound on Mechanical Properties of Porcine Carotid Arteries Post-Angioplasty." In ASME 2019 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/imece2019-11661.

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Abstract Percutaneous transluminal angioplasty (PTA) is a medical procedure performed on patients with severe atherosclerosis to open up stenosed blood vessels by inflating a balloon at the narrowing location. In many cases of PTA, restenosis occurs post-surgery due either to elastic behavior of the artery, also known as elastic recoil in medical literature, or to plaque reformation within the lumen. For that reason, stents are commonly deployed to keep the arterial lumen open. Stent deployment causes problems in some cases; for example, the presence of stents in arteries with frequent movements and large deformations can cause ruptures in the arterial wall. Recent studies on 1,8-Naphthalimide organic compounds have shown that when these compounds are activated using a certain wavelength of light, it causes cross-linking between the components of the extracellular matrix. This observation has led to studies with the goal of developing a method to utilize this process to replace stents for cases with limiting conditions for stent deployment. In this study we focused on measuring and quantifying the effects of this compound on the mechanical properties of treated arteries undergoing PTA under a variety of loading conditions.
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Gebreegziabher, T., E. Ayorinde, and T. Singh. "Detection and Characterization of Pulsatile Flow Induced Acoustic Emissions in Stenosed Arterial Geometric Models." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39914.

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A Newtonian fluid is used in a simplified experimental hydraulic model of a cardiovascular system (CVS) to study pulsatile flow in arterial geometric models with different stages of stenosis (restriction rates) and understand the progression of stenosis and how the fluid flow properties in stenosed sections of arteries behave. In this study, 16mm long cylindrical stenosis models (orifices) with different restriction rates were pressed into the middle section of a 570 mm long arterial geometric model (polyethylene tube) one at a time. The arterial geometric models were connected to a solenoid or reciprocating pump (DC Voltage) capable of generating pulsatile flow at different pumping frequencies. The effects of pulsatile flow properties (pressure pulse, flow rate, etc) on acoustic emission (AE) signal levels using sensors for the detection of elastic waves in the arterial models for different restriction rates of stenoitic geometric models (orifices) at different pumping frequencies have been investigated. The results from this research show that there is a strong correlation between the flow properties of the Newtonian fluid in the arterial geometric models and the level of the flow induced AE signal indicators such as the waveforms, elastic energy, number of events, etc. Thus, as AE techniques can be used to predict flow characteristics in a given geometric model to assess the restriction level of a flow passage, the same principle could be applied in the detection of severe atherosclerosis or stenosis in large arteries — human external carotid arteries.
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Wan, William, Hiromi Yanagisawa, and Rudolph L. Gleason. "Biomechanical and Microstructural Properties of Fibulin-5 Null Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206435.

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Fibulin-5 is an extracellular matrix (ECM) protein that interacts with integrins and plays a critical role in organizing elastic fibers. Gross observation and histological examination reveal that carotid arteries from fibulin-5 knockout (fib5-/-) mice have disrupted elastic lamellae and are more tortuous [1]. The properties of fibulin-5 null mice provide a unique platform for developing constituent based models for vascular mechanics. While numerous models for blood vessels exist, there is a need to relate measurable microstructural metrics of structurally-based constitutive relations. We performed mechanical tests on carotid arteries from wildtype (WT) and fib5-/-mice and imaged live vessels under multiple loading scenarios to quantify microstructure during deformation. We also fit experimental results to a constitutive relation based on Holzapfel’s model [2]. These results provide a basis for further model development.
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Gruber, Matthew J., Varun Krishnamurthy, D. A. Narmoneva, and Robert B. Hinton. "Elastin Haploinsufficiency Is Associated With Altered Interstitial Phenotype and Progressive Aortopathy." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192891.

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Supravalvular aortic stenosis (SVAS) [1] is a disease of the cardiovascular system that leads to narrowing of the large arteries in humans. Studies have shown [2] that SVAS is caused by mutations or deletions in the elastin gene resulting in elastin haploinsufficiency. Elastin haploinsufficiency results in systemic hypertension [3], thinner and more numerous elastic lamellae [4], and altered arterial mechanics [5]. Genetically modified elastin deficient mice (ELN+/-) recapitulates the human phenotype including obstructive arterial disease and decreased arterial compliance [1,3]. Elastin deficiency in these mice is associated with changes in the mechanical microenvironment in the vascular wall [6], including enhanced wall thickness, increased smooth muscle cell (SMC) proliferation [7] and stiffening of arteries [8]. However, the molecular mechanisms for these changes are not fully understood. Also from a developmental perspective, no information is available regarding initiation and progression of aortic pathology in ELN+/− mice with time. The objectives of this study were to determine the temporal effects of elastin haploinsufficiency on the functional properties of aortic tissue and the aortic cell phenotype, using the elastin deficient mouse model (ELN+/-). We hypothesized that elastin haploinsufficiency will result in progressive abnormalities in aortic stiffness and dynamic alterations in aortic smooth muscle cell phenotype.
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