Residual stress and strain in the lamellar unit of the porcine aorta: experiment and analysis

Matsumotο, Takeo; Goto, Tadahiko; Furukawa, Takashi; Sato, Masaaki

doi:10.1016/j.jbiomech.2003.08.014

Cited by 77 publications

(54 citation statements)

References 10 publications

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“…It would be interesting to know how normal moduli relate to shear moduli. This knowledge may also be important in determining the shear modulus of the smooth muscle-rich layer in the lamellar unit of aortas, whose significance in blood-vessel wall micromechnanics has been argued recently (23), (24) .…”

Section: Discussionmentioning

confidence: 98%

Mechanical Anisotropy of Rat Aortic Smooth Muscle Cells Decreases with Their Contraction (Possible Effect of Actin Filament Orientation)

Nagayama

Matsumotο

2004

JSME Int. J., Ser. C

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Tensile properties of smooth muscle cells freshly isolated from rat thoracic aortas (FSMCs) in their major and minor axes were measured using a laboratory-made micro tensile tester. The relationship between the tension applied to a cell and its elongation was obtained in untreated cells and those treated with 10 −5 M serotonin to induce contraction. An initial stiffness of untreated FSMCs, normalized by their initial cross-sectional area perpendicular to the stretch direction, was significantly higher in the major axis (14.8 ± 4.3 kPa, mean ± SEM, n = 5) than the minor axis (2.8 ± 1.0 kPa, n = 5). The stiffness increased significantly in response to the contraction, but the increase was much higher in the minor axis (59.0±9.4 kPa, n = 4) than in the major (88.1±13.3 kPa, n = 4). The difference between the two directions was insignificant in the contracted state. Observations of the morphology of actin filaments with a confocal laser scanning microscope in untreated FSMCs revealed that they were long fibers running almost parallel to the major axis, while those in contracted cells showed an aggregated structure without a preferential direction. These results may indicate that anisotropy in untreated FSMCs is caused by the anisotropic alignment of their actin filaments, and that such anisotropy disappears in response to actin filament reorganization caused by the contraction.

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Section: Discussionmentioning

confidence: 98%

Mechanical Anisotropy of Rat Aortic Smooth Muscle Cells Decreases with Their Contraction (Possible Effect of Actin Filament Orientation)

Nagayama

Matsumotο

2004

JSME Int. J., Ser. C

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“…And also, we need to examine the residual stress in the wall, especially at a microscopic level. Recently, we found that residual stresses still resided even in a plate-like segment of aorta at a microscopic level (17), (18) . By measuring residual stress in the smooth muscle and elastic layers separately, we may be able to know the cause of the changes in the mechanical properties in more detail.…”

Section: Limitations and Future Studymentioning

confidence: 99%

Flow-Induced Changes in Dimensions and Mechanical Properties of Rabbit Common Carotid Arteries

Matsumotο

Okumura

Shirono

et al. 2005

JSME Int. J., Ser. C

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Flow-induced changes in dimensions and mechanical properties of blood vessel wall were studied in the rabbit left common carotid arteries connected directly to the left external jugular vein via an arteriovenous fistula (AVF) to increase its blood flow by >10-fold for 4 weeks. Contralateral artery was used as control. We found significant increase not only in diameter, but also in thickness and length of unloaded artery exposed to increased flow, indicating the increase in wall volume. The increase in diameter and thickness but not in longitudinal length correlated significantly with the volumetric increase of the wall. Pressure-imposed test showed that the wall became less distensible in response to flow increase. Fluid shear stress estimated for physiological condition was significantly higher in AVF side than control, indicating that 10-fold increase in flow was not compensated in 4 weeks. Circumferential strain in a physiological pressure range was significantly lower in AVF side, while hoop stress was similar in both sides. These results may indicate that circumferential stress but not strain is maintained constant, and longitudinal change is not regulated in flow-imposed arteries.

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“…In spite of such material heterogeneity, the above experimental protocol can be used to release most of the RS/S in the pathological vessel. The resultant open configuration of the atherosclerotic vessel is assumed to be free of stress and has therefore been called by Matsumoto et al (39) the "macroscopic stress-free configuration," although admittedly other lower-amplitude RS/S patterns might still be at work in the plaque even after radial sectioning (40).…”

Section: Background: Idealized Case Illustrating the Importance Of Rsmentioning

confidence: 99%

Influence of residual stress/strain on the biomechanical stability of vulnerable coronary plaques: potential impact for evaluating the risk of plaque rupture

Ohayon¹,

Dubreuil²,

Tracqui³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

108

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In a vulnerable plaque (VP), rupture often occurs at a site of high stress within the cap. It is also known that vessels do not become free of stress when all external loads are removed. Previous studies have shown that such residual stress/strain (RS/S) tends to make the stress distribution more uniform throughout the media of a normal artery. However, the influence of RS/S on the wall stress distribution in pathological coronaries remains unclear. The aim of this study was to investigate the effects of RS/S on the biomechanical stability of VPs. RS/S patterns were studied ex vivo in six human vulnerable coronary plaque samples. Because the existence of RS/S can only be assessed by releasing it, the opening angle technique was the experimental approach used to study the geometrical opening configurations of the diseased arteries, producing an arterial wall in a near-zero stress state. Reciprocally, these opening geometries were used in finite element simulations to reconstruct the RS/S distributions in closed arteries. It was found that the RS/S 1) is not negligible, 2) dramatically affects the physiological peak stress amplitude in the thin fibrous cap, 3) spotlights some new high stress areas, and 4) could be a landmark of the lipid core's developmental process within a VP. This study demonstrates that plaque rupture is not to be viewed as a consequence of intravascular pressure alone, but rather of a subtle combination of external loading and intraplaque RS/S.

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Residual stress and strain in the lamellar unit of the porcine aorta: experiment and analysis

Cited by 77 publications

References 10 publications

Mechanical Anisotropy of Rat Aortic Smooth Muscle Cells Decreases with Their Contraction (Possible Effect of Actin Filament Orientation)

Mechanical Anisotropy of Rat Aortic Smooth Muscle Cells Decreases with Their Contraction (Possible Effect of Actin Filament Orientation)

Flow-Induced Changes in Dimensions and Mechanical Properties of Rabbit Common Carotid Arteries

Influence of residual stress/strain on the biomechanical stability of vulnerable coronary plaques: potential impact for evaluating the risk of plaque rupture

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