Material Properties of Rat Middle Cerebral Arteries at High Strain Rates

Bell, E. David; Converse, Matthew I.; Mao, Haojie; Unnikrishnan, Ginu; Reifman, Jaques; Monson, Kenneth L.

doi:10.1115/1.4039625

Cited by 12 publications

(6 citation statements)

References 29 publications

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“…We obtained the material properties of the face and skull from the literature, consistent with previous blast simulations of the rat head 19. We derived the material properties of the brain and cerebral vasculature from recent high-strain-rate studies of these tissues for male Sprague–Dawley rats 1,8. To account for regional variations in the material properties of the rat brain, we divided the brain into three regions: the cerebrum, cerebellum, and brainstem.…”

Section: Discussionmentioning

confidence: 99%

“…Similar to those of brain tissues, the material properties of the cerebral vasculature were based on high-strain-rate axial tensile testing of the middle cerebral arteries of male Sprague–Dawley rats up to a maximum strain rate of 500 s −1 (Supplementary Fig. 2) 1…”

Section: Methodsmentioning

confidence: 99%

“…Similarly, Bell et al . performed high-strain-rate tensile testing of the middle cerebral arteries from male Sprague–Dawley rats 1. The study, which was performed at strain rates ranging from quasi-static to 1000 s −1 , showed rate-dependency in the material properties of the cerebral vasculature at strain rates beyond 700 s −1 .…”

Section: Introductionmentioning

confidence: 99%

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A 3-D Rat Brain Model for Blast-Wave Exposure: Effects of Brain Vasculature and Material Properties

et al. 2019

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Exposure to blast waves is suspected to cause primary traumatic brain injury. However, existing finite-element (FE) models of the rat head lack the necessary fidelity to characterize the biomechanical responses in the brain due to blast exposure. They neglect to represent the cerebral vasculature, which increases brain stiffness, and lack the appropriate brain material properties characteristic of high strain rates observed in blast exposures. To address these limitations, we developed a high-fidelity three-dimensional FE model of a rat head. We explicitly represented the rat’s cerebral vasculature and used high-strain-rate material properties of the rat brain. For a range of blast overpressures (100 to 230 kPa) the brain-pressure predictions matched experimental results and largely overlapped with and tracked the incident pressure–time profile. Incorporating the vasculature decreased the average peak strain in the cerebrum, cerebellum, and brainstem by 17, 33, and 18%, respectively. When compared with our model based on rat-brain properties, the use of human-brain properties in the FE model led to a three-fold reduction in the strain predictions. For simulations of blast exposure in rats, our findings suggest that representing cerebral vasculature and species-specific brain properties has a considerable influence in the resulting brain strain but not the pressure predictions.Electronic supplementary materialThe online version of this article (10.1007/s10439-019-02277-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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A 3-D Rat Brain Model for Blast-Wave Exposure: Effects of Brain Vasculature and Material Properties

et al. 2019

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“…We used a one-term Ogden model to capture the deviatoric response of the vasculature wall (Unnikrishnan et al, 2019). We obtained these properties (Table 1) from high-strain-rate axial testing of the middle cerebral arteries of male Sprague-Dawley rats (Bell et al, 2018). Because these experiments showed no difference between the response of arteries tested at quasi-static conditions and those tested at high strain rates relevant to blast exposure (<500 s −1 ), we did not account for the viscoelastic behavior of the vessels in our material model.…”

Section: Materials Propertiesmentioning

confidence: 99%

Does Blast Exposure to the Torso Cause a Blood Surge to the Brain?

Rubio

Skotak

Alay

et al. 2020

Front. Bioeng. Biotechnol.

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The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (<1%). In summary, our analyses show that the indirect mechanism causes a sudden and abundant stream of blood to rapidly propagate from the torso through the neck to the cerebral vasculature. This blood surge causes a considerable increase in the wall shear stresses in the brain vasculature network, which may lead to functional and structural effects on the cerebral veins and arteries, ultimately leading to vascular pathology. In contrast, our findings do not support the notion of strain-induced brain-tissue damage due to the indirect mechanism.

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“…These approaches represent important milestones that need to be considered as pre-cursors to eventual longitudinal in vivo curvature assessment of the aortic valve leaflets. In addition, valve tissue stiffness has been shown to be a function of the strain rate and frequency [23,24,25,26], specifically that a faster rate of deformation will yield a higher tissue stiffness. In the present study, leaflet strip curvature was assessed while the frequency was held constant at a physiologically-relevant magnitude of 1 Hz.…”

Section: Limitationsmentioning

confidence: 99%

Elastin-Dependent Aortic Heart Valve Leaflet Curvature Changes During Cyclic Flexure

et al. 2019

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The progression of calcific aortic valve disease (CAVD) is characterized by extracellular matrix (ECM) remodeling, leading to structural abnormalities and improper valve function. The focus of the present study was to relate aortic valve leaflet axial curvature changes as a function of elastin degradation, which has been associated with CAVD. Circumferential rectangular strips (L × W = 10 × 2.5 mm) of normal and elastin-degraded (via enzymatic digestion) porcine AV leaflets were subjected to cyclic flexure (1 Hz). A significant increase in mean curvature (p < 0.05) was found in elastin-degraded leaflet specimens in comparison to un-degraded controls at both the semi-constrained (50% of maximum flexed state during specimen bending and straightening events) and fully-constrained (maximally-flexed) states. This significance did not occur in all three flexed configurations when measurements were performed using either minimum or maximum curvature. Moreover, the mean curvature increase in the elastin-degraded leaflets was most pronounced at the instance of maximum flexure, compared to un-degraded controls. We conclude that the mean axial curvature metric can detect distinct spatial changes in aortic valve ECM arising from the loss in bulk content and/or structure of elastin, particularly when there is a high degree of tissue bending. Therefore, the instance of maximum leaflet flexure during the cardiac cycle could be targeted for mean curvature measurements and serve as a potential biomarker for elastin degradation in early CAVD remodeling.

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Material Properties of Rat Middle Cerebral Arteries at High Strain Rates

Cited by 12 publications

References 29 publications

A 3-D Rat Brain Model for Blast-Wave Exposure: Effects of Brain Vasculature and Material Properties

A 3-D Rat Brain Model for Blast-Wave Exposure: Effects of Brain Vasculature and Material Properties

Does Blast Exposure to the Torso Cause a Blood Surge to the Brain?

Elastin-Dependent Aortic Heart Valve Leaflet Curvature Changes During Cyclic Flexure

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