Effect of Storage Duration on the Mechanical Behavior of Mouse Carotid Artery

Amin, Mazyar; Kunkel, Amber G.; Le, Victoria; Wagenseil, Jessica E.

doi:10.1115/1.4004415

Cited by 21 publications

(14 citation statements)

References 13 publications

(22 reference statements)

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“…AAs were stored in physiologic saline solution at 4°C for up to two days before testing (Amin et al 2011). The AA was mounted in a 37°C Myograph 110P (Danish Myotechnology) bath filled with physiologic saline solution, stretched axially to 1.05 times the unloaded length, and preconditioned by pressurizing for three cycles from 0 – 60 mmHg at a constant rate (4 mmHg/sec).…”

Section: Methodsmentioning

confidence: 99%

Crosslinked elastic fibers are necessary for low energy loss in the ascending aorta

Kim

Staiculescu

Cocciolone

et al. 2017

Journal of Biomechanics

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In the large arteries, it is believed that elastin provides the resistance to stretch at low pressure, while collagen provides the resistance to stretch at high pressure. It is also thought that elastin is responsible for the low energy loss observed with cyclic loading. These tenets are supported through experiments that alter component amounts through protease digestion, vessel remodeling, normal growth, or in different artery types. Genetic engineering provides the opportunity to revisit these tenets through the loss of expression of specific wall components. We used newborn mice lacking elastin (Eln−/−) or two key proteins (lysyl oxidase, Lox−/−, or fibulin-4, Fbln4−/−) that are necessary for the assembly of mechanically-functional elastic fibers to investigate the contributions of elastic fibers to large artery mechanics. We determined component content and organization and quantified the nonlinear and viscoelastic mechanical behavior of Eln−/−, Lox−/−, and Fbln4−/− ascending aorta and their respective controls. We confirmed that the lack of elastin, fibulin-4, or lysyl oxidase leads to absent or highly fragmented elastic fibers in the aortic wall and a 56 – 97% decrease in crosslinked elastin amounts. We found that the resistance to stretch at low pressure is decreased only in Eln−/− aorta, confirming the role of elastin in the nonlinear mechanical behavior of the aortic wall. Dissipated energy with cyclic loading and unloading is increased 53 – 387% in Eln−/−, Lox−/−, and Fbln4−/− aorta, indicating that not only elastin, but properly assembled and crosslinked elastic fibers, are necessary for low energy loss in the aorta.

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Section: Methodsmentioning

confidence: 99%

Crosslinked elastic fibers are necessary for low energy loss in the ascending aorta

Kim

Staiculescu

Cocciolone

et al. 2017

Journal of Biomechanics

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“…All protocols were approved by the Institutional Animal Care and Use Committee. Mice were sacrificed by CO 2 inhalation, then the right and left carotid arteries were removed, placed in physiological saline solution (PSS), stored at 4° C, and used for mechanical tests within three days (Amin et al 2011). Mechanical tests were performed with each carotid mounted in a pressure myograph system (Danish Myotechnology) in PSS at 37° C (Wagenseil et al 2005).…”

Section: Methodsmentioning

confidence: 99%

Critical buckling pressure in mouse carotid arteries with altered elastic fibers

Luetkemeyer

James

Devarakonda

et al. 2015

Journal of the Mechanical Behavior of Biomedical Materials

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Arteries can buckle axially under applied critical buckling pressure due to a mechanical instability. Buckling can cause arterial tortuosity leading to flow irregularities and stroke. Genetic mutations in elastic fiber proteins are associated with arterial tortuosity in humans and mice, and may be the result of alterations in critical buckling pressure. Hence, the objective of this study is to investigate how genetic defects in elastic fibers affect buckling pressure. We use mouse models of human disease with reduced amounts of elastin (Eln+/−) and with defects in elastic fiber assembly due to the absence of fibulin-5 (Fbln5−/−). We find that Eln+/− arteries have reduced buckling pressure compared to their wild-type controls. Fbln5−/− arteries have similar buckling pressure to wild-type at low axial stretch, but increased buckling pressure at high stretch. We fit material parameters to mechanical test data for Eln+/−, Fbln5−/− and wild-type arteries using Fung and four-fiber strain energy functions. Fitted parameters are used to predict theoretical buckling pressure based on equilibrium of an inflated, buckled, thick-walled cylinder. In general, the theoretical predictions underestimate the buckling pressure at low axial stretch and overestimate the buckling pressure at high stretch. The theoretical predictions with both models replicate the increased buckling pressure at high stretch for Fbln5−/− arteries, but the four-fiber model predictions best match the experimental trends in buckling pressure changes with axial stretch. This study provides experimental and theoretical methods for further investigating the influence of genetic mutations in elastic fibers on buckling behavior and the development of arterial tortuosity.

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“…All protocols were approved by the Institutional Animal Care and Use Committee. Each aorta was excised and stored in physiologic saline solution (PSS) for 0–3 days before testing (Amin et al 2011). For testing, each aorta was mounted in the myograph in PSS at 37 °C (Wagenseil et al 2005) and subjected to three constant-length inflation cycles and three constant-pressure axial stretch cycles (Table 1).…”

Section: Methodsmentioning

confidence: 99%

A fiber-based constitutive model predicts changes in amount and organization of matrix proteins with development and disease in the mouse aorta

Cheng

Stoilov

Mecham

et al. 2012

Biomech Model Mechanobiol

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Decreased elastin in mice (Eln+/−) yields a functioning vascular system with elevated blood pressure and increased arterial stiffness that is morphologically distinct from wild-type mice (WT). Yet, function is retained enough that there is no appreciable effect on life span and some mechanical properties are maintained constant. It is not understood how the mouse modifies the normal developmental process to produce a functioning vascular system despite a deficiency in elastin. To quantify changes in mechanical properties, we have applied a fiber-based constitutive model to mechanical data from the ascending aorta during postnatal development of WT and Eln+/− mice. Results indicate that the fiber-based constitutive model is capable of distinguishing elastin amounts and identifying trends during development. We observe an increase in predicted circumferential stress contribution from elastin with age, which correlates with increased elastin amounts from protein quantification data. The model also predicts changes in the unloaded collagen fiber orientation with age, which must be verified in future work. In Eln+/− mice, elastin amounts are decreased at each age, along with the predicted circumferential stress contribution of elastin. Collagen amounts in Eln+/− aorta are comparable to WT, but the predicted circumferential stress contribution of collagen is increased. This may be due to altered organization or structure of the collagen fibers. Relating quantifiable changes in arterial mechanics with changes in extracellular matrix (ECM) protein amounts will help in understanding developmental remodeling and in producing treatments for human diseases affecting ECM proteins.

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Effect of Storage Duration on the Mechanical Behavior of Mouse Carotid Artery

Cited by 21 publications

References 13 publications

Crosslinked elastic fibers are necessary for low energy loss in the ascending aorta

Crosslinked elastic fibers are necessary for low energy loss in the ascending aorta

Critical buckling pressure in mouse carotid arteries with altered elastic fibers

A fiber-based constitutive model predicts changes in amount and organization of matrix proteins with development and disease in the mouse aorta

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