Elastase, collagenase, and the biaxial elastic properties of dog carotid artery

Dobrin, Philip B.; Canfield, Thomas R.

doi:10.1152/ajpheart.1984.247.1.h124

Cited by 76 publications

(79 citation statements)

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“…Dobrin and coworkers found that there was no change in axial compliance with collagenase treatment, contradicting the results of this study [49,50]. However Gundiah et al found collagenase treatment affected wall compliance in both directions, which supports the findings here [18].…”

Section: Collagenase Treatmentcontrasting

confidence: 81%

Creating a model of diseased artery damage and failure from healthy porcine aorta

Noble

Smulders

Green

et al. 2016

Journal of the Mechanical Behavior of Biomedical Materials

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Article available under the terms of the CC-BY-NC-ND licence (https://creativecommons.org/licenses/by-nc-nd/4.0/) eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request.Creating a model of diseased artery damage and failure from healthy porcine aorta AbstractLarge quantities of diseased tissue are required in the research and development of new generations of medical devices, for example for use in physical testing. However, these are difficult to obtain. In contrast, porcine arteries are readily available as they are regarded as waste. Therefore, reliable means of creating from porcine tissue physical models of diseased human tissue that emulate well the associated mechanical changes would be valuable. To this end, we studied the effect on mechanical response of treating porcine thoracic aorta with collagenase, elastase and glutaraldehyde. The alterations in mechanical and failure properties were assessed via uniaxial tension testing. A constitutive model composed of the Gasser-Ogden-Holzapfel model, for elastic response, and a continuum damage model, for the failure, was also employed to provide a further basis for comparison [1,2]. For the concentrations used here it was found that: collagenase treated samples showed decreased fracture stress in the axial direction only; elastase treated samples showed increased fracture stress in the circumferential direction only; and glutaraldehyde samples showed no change in either direction. With respect to the proposed constitutive model, both collagenase and elastase had a strong effect on the fibre-related terms. The model more closely captured the tissue response in the circumferential direction, due to the smoother and sharper transition from damage initiation to complete failure in this direction. Finally, comparison of the results with those of tensile tests on diseased tissues suggests these treatments indeed provide a basis for creation of physical models of diseased arteries.

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Section: Collagenase Treatmentcontrasting

confidence: 81%

Creating a model of diseased artery damage and failure from healthy porcine aorta

Noble

Smulders

Green

et al. 2016

Journal of the Mechanical Behavior of Biomedical Materials

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“…It is generally accepted that under conditions of low wall strain, elastin is the primary load-bearing component of the vascular wall and that as wall strain increases collagen plays a more prominent role in supporting passive wall tension (1,8,16). For example, Dobrin and Canfield (16) examined the passive biaxial mechanical behavior of dog carotid arteries following treatment with elastase or collagenase.…”

Section: Functional Relevance Of Relaxin-induced Vascular Wall Remodementioning

confidence: 99%

Relaxin regulates vascular wall remodeling and passive mechanical properties in mice

Debrah

Haney

et al. 2011

Journal of Applied Physiology

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Administration of recombinant human relaxin (rhRLX) to conscious rats increases global arterial compliance, and small renal arteries (SRA) isolated from these rats demonstrate increased passive compliance. Here we characterize relaxin-induced vascular remodeling and examine its functional relevance. SRA and external iliac arteries (EIA) were examined in rhRLX-treated (1.0 g/h for 5 days) and relaxin knockout mice. Arterial geometric remodeling and compositional remodeling were quantified using immunohistochemical and biochemical techniques. Vascular mechanical properties were quantified using an ex vivo preparation wherein pressure-diameter data were obtained at various axial lengths. Compared with vehicle-treated mice, SRA from rhRLX-treated mice showed outward geometric remodeling (increased unstressed wall area and wall-to-lumen area ratio), increased smooth muscle cell (SMC) density, reduction in collagen-to-total protein ratio, and unchanged elastin-to-tissue dry weight ratio. Compared with wild-type mice, relaxin knockout mice exhibited the opposite pattern: decreased unstressed wall area and wall-to-lumen area ratio, decreased SMC density, and increased collagen-to-total protein ratio. Although tissue biaxial strain energy of SRA was not different between rhRLX-and vehicle-treated groups at low-to-physiological circumferential and axial strains, it was lower for the rhRLX-treated group at the highest circumferential strain. In contrast to SRA, relaxin administration was not associated with any vascular remodeling or changes in passive mechanics of EIA. Thus relaxin induces both geometric and compositional remodeling in vessel-specific manner. Relaxin-induced geometric remodeling of SRA is responsible for the increase in passive compliance under low-to-physiological levels of circumferential and axial strains, and compositional remodeling becomes functionally relevant only under high circumferential strain. arterial compliance; arterial collagen; elastin; smooth muscle; matrix metalloproteinase-2; relaxin knockout mice RELAXIN IS A 6-KDA PEPTIDE hormone that emanates from the corpus luteum and circulates during the luteal phase of the menstrual cycle and in pregnancy (42). Traditionally, the hormone has been associated with the female reproductive tract, but recent evidence indicates that relaxin plays an important role in cardiovascular function (reviewed in Refs. 7, 28). We found that administration of recombinant human relaxin (rhRLX) to chronically instrumented, nonpregnant female and male rats increased cardiac output and global arterial compliance (AC), as well as decreased systemic vascular resistance (6,13,14). Concurrent with relaxin's influence on overall cardiovascular function, small renal arteries isolated from the rhRLX-treated, nonpregnant female rats demonstrated increased passive compliance (6). More recently, we explored the role of endogenous, vascular-derived relaxin in modifying arterial mechanical properties in mice. We observed that small renal arteries isolated from relaxin knockout...

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“…These data are therefore helpful to develop the SEF of different wall constituents. Among models with selectively altered constituents, elastase-treated arteries offer an attractive model to access the biomechanical properties of arteries after elastin degradation, as seen in pathologies such as aortic stiffening with age and aneurysm formation (Dobrin 1989;Dobrin and Canfield 1984;Hayashi et al 1987). Recently, Fonck et al studied the collagen engagement profile in intact and elastase-treated arteries by applying the SEF proposed by Zulliger et al on P-r o curves and suggested a clear interaction between collagen and elastin in the arterial wall (Fonck et al 2007).…”

Section: Elastin 3d Ultrastructure In Arteriesmentioning

confidence: 99%

Role of elastin anisotropy in structural strain energy functions of arterial tissue

Rezakhaniha

Fonck

Genoud

et al. 2010

Biomech Model Mechanobiol

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The vascular wall exhibits nonlinear anisotropic mechanical properties. The identification of a strain energy function (SEF) is the preferred method to describe its complex nonlinear elastic properties. Earlier constituent-based SEF models, where elastin is modeled as an isotropic material, failed in describing accurately the tissue response to inflation-extension loading. We hypothesized that these shortcomings are partly due to unaccounted anisotropic properties of elastin. We performed inflation-extension tests on common carotid of rabbits before and after enzymatic degradation of elastin and applied constituent-based SEFs, with both an isotropic and an anisotropic elastin part, on the experimental data. We used transmission electron microscopy (TEM) and serial block-face scanning electron microscopy (SBFSEM) to provide direct structural evidence of the assumed anisotropy. In intact arteries, the SEF including anisotropic elastin with one family of fibers in the circumferential direction fitted better the inflation-extension data than the isotropic SEF. This was supported by TEM and SBFSEM imaging, which showed interlamellar elastin fibers in the circumferential direction. In elastin-degraded arteries, both SEFs succeeded equally well in predicting anisotropic wall behavior. In elastase-treated arteries fitted with the anisotropic SEF for elastin, collagen engaged later than in intact arteries. We conclude that constituent-based models with an anisotropic elastin part characterize more accurately the mechanical properties of the arterial wall when compared to models with simply an isotropic elastin. Microstructural imaging based on electron microscopy techniques provided evidence for elastin anisotropy. Finally, the model suggests a later and less abrupt collagen engagement after elastase treatment.

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Elastase, collagenase, and the biaxial elastic properties of dog carotid artery

Cited by 76 publications

References 0 publications

Creating a model of diseased artery damage and failure from healthy porcine aorta

Creating a model of diseased artery damage and failure from healthy porcine aorta

Relaxin regulates vascular wall remodeling and passive mechanical properties in mice

Role of elastin anisotropy in structural strain energy functions of arterial tissue

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