Research Papers

Material Properties of Rat Middle Cerebral Arteries at High Strain Rates

[+] Author and Article Information
E. David Bell

Department of Bioengineering,
University of Utah,
Salt Lake City, UT 84112

Matthew Converse

Department of Mechanical Engineering,
University of Utah,
Salt Lake City, UT 84112

Haojie Mao

Telemedicine and Advanced Technology
Research Center,
Department of Defense Biotechnology High
Performance Computing Software
Applications Institute,
U.S. Army Medical Research and
Materiel Command,
Frederick, MD 21702

Ginu Unnikrishnan

Telemedicine and Advanced Technology Research Center,
Department of Defense Biotechnology High
Performance Computing Software
Applications Institute,
U.S. Army Medical Research and
Materiel Command,
Frederick, MD 21702

Jaques Reifman

Telemedicine and Advanced Technology Research Center,
Department of Defense Biotechnology High
Performance Computing Software Applications
U.S. Army Medical Research and
Materiel Command,
Frederick, MD 21702

Kenneth L. Monson

Department of Bioengineering,
University of Utah,
Salt Lake City, UT 84112;
Department of Mechanical Engineering,
University of Utah,
1495 E. 100 S., MEK 1550,
Salt Lake City, UT 84112
e-mail: ken.monson@utah.edu

1Corresponding author.

Manuscript received October 4, 2017; final manuscript received February 20, 2018; published online April 19, 2018. Assoc. Editor: Barclay Morrison.

J Biomech Eng 140(7), 071004 (Apr 19, 2018) (7 pages) Paper No: BIO-17-1446; doi: 10.1115/1.4039625 History: Received October 04, 2017; Revised February 20, 2018

Traumatic brain injury (TBI), resulting from either impact- or nonimpact blast-related mechanisms, is a devastating cause of death and disability. The cerebral blood vessels, which provide critical support for brain tissue in both health and disease, are commonly injured in TBI. However, little is known about how vessels respond to traumatic loading, particularly at rates relevant to blast. To better understand vessel responses to trauma, the objective of this project was to characterize the high-rate response of passive cerebral arteries. Rat middle cerebral arteries (MCAs) were isolated and subjected to high-rate deformation in the axial direction. Vessels were perfused at physiological pressures and stretched to failure at strain rates ranging from approximately 100 to 1300 s−1. Although both in vivo stiffness and failure stress increased significantly with strain rate, failure stretch did not depend on rate.

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Grahic Jump Location
Fig. 2

(a) Diagram of mass-spring-damper system used to model load cell. Applied load from blood vessel (FBV) is to the right; output load (FLC) is to the left. (b) Force-time plot of vessel force predicted by reverse simulation in a representative medium strain rate test (∼500 s−1). The predicted vessel force was subsequently validated through direct measurement using a piezoelectric force transducer.

Grahic Jump Location
Fig. 1

Schematic of the high-rate testing apparatus. Vessel deformation was observed through a viewing window (VW). The left end of the vessel was fixed to the stationary load cell (LC), which was mounted to a vibration-damping cork base (CB) through an XY positioning stage (XY). The right end of the vessel displaced rapidly when the sled (S) was accelerated by the steel cable extending to the base of the drop tube (not shown). Rigid limits (L) were imposed to bound movement of the sled and prevent damage to the apparatus.

Grahic Jump Location
Fig. 3

Representative axial Cauchy stress-stretch curves for all groups, including high (>700 s−1; HR), medium (400–500 s−1; MR), and low (100–200 s−1; LR) strain rate cases. The internal pressure was fixed at 6.7 kPa for specimens indicated by open circles; for all others, it was fixed at 13.3 kPa. These representative cases suggest trends toward higher stresses and lower stretches with higher strain rates; there is no apparent effect of pressure.

Grahic Jump Location
Fig. 4

Stretch and Cauchy stress as a function of time for representative cases. Strain rates are indicated over in vivo (1.05–1.15) and large (1.30–1.40) stretch ranges for each stretch curve. These data show that the strain rate at the in vivo stretch was 60% of that at larger stretches.

Grahic Jump Location
Fig. 5

(a) In vivo stiffness, (b) Max first P-K stress (failure stress), and (c) stretch at maximum first P-K stress as a function of strain rate (calculated over the in vivo region), including quasi-static data from the previously reported experiments [22]. Despite the significant scatter, these plots show trends of increasing stiffness and failure stress with strain rate. Stretch at maximum stress appears to be independent of rate.

Grahic Jump Location
Fig. 6

Mean (±standard deviation): (a) axial in vivo stiffness, (b) maximum first Piola–Kirchhoff (first P-K) stress, and (c) stretch at maximum first P-K stress for the quasi-static (QS), Low, Med, and High rate groups. Solid and dashed brackets indicate statistically different groups for the three- and four-group comparisons, respectively. These figures confirm statistically significant rate sensitivity for in vivo stiffness and failure stress but not for failure stretch.



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