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Technical Briefs

Effect of Strain Rate on the Material Properties of Human Liver Parenchyma in Unconfined Compression

[+] Author and Article Information
Andrew R. Kemper

e-mail: akemper@vt.edu

Stefan M. Duma

Center for Injury Biomechanics,
Virginia Tech—Wake Forest University,
Blacksburg, VA 24061

1Corresponding author.

Contributed by the Bioengineering Division of ASME for publication in the Journal of Biomechanical Engineering. Manuscript received May 30, 2012; final manuscript received May 29, 2013; accepted manuscript posted June 17, 2013; published online September 20, 2013. Editor: Victor H. Barocas.

J Biomech Eng 135(10), 104503 (Sep 20, 2013) (8 pages) Paper No: BIO-12-1214; doi: 10.1115/1.4024821 History: Received May 30, 2012; Revised May 29, 2013; Accepted June 17, 2013

The liver is one of the most frequently injured organs in abdominal trauma. Although motor vehicle collisions are the most common cause of liver injuries, current anthropomorphic test devices are not equipped to predict the risk of sustaining abdominal organ injuries. Consequently, researchers rely on finite element models to assess the potential risk of injury to abdominal organs such as the liver. These models must be validated based on appropriate biomechanical data in order to accurately assess injury risk. This study presents a total of 36 uniaxial unconfined compression tests performed on fresh human liver parenchyma within 48 h of death. Each specimen was tested once to failure at one of four loading rates (0.012, 0.106, 1.036, and 10.708 s−1) in order to investigate the effects of loading rate on the compressive failure properties of human liver parenchyma. The results of this study showed that the response of human liver parenchyma is both nonlinear and rate dependent. Specifically, failure stress significantly increased with increased loading rate, while failure strain significantly decreased with increased loading rate. The failure stress and failure strain for all liver parenchyma specimens ranged from −38.9 kPa to −145.9 kPa and from −0.48 strain to −1.15 strain, respectively. Overall, this study provides novel biomechanical data that can be used in the development of rate dependent material models and the identification of tissue-level tolerance values, which are critical to the validation of finite element models used to assess injury risk.

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Figures

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Fig. 1

Preliminary histology study performed on bovine liver parenchyma to evaluate the tissue preservation methodology

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Fig. 2

Specimen slicing methodology (a) square block of parenchyma placed in the slicing jig, (b) blades aligned with guide slots in the slicing jig, (c) slicing performed in one smooth pass to produce multiple slices, and (d) exemplar constant 10 mm thick slice of liver parenchyma

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Fig. 3

Specimen cutting methodology (a) constant thickness parenchyma slice placed on the cutting base, (b) template placed over the slice to obtain a specimen devoid of any visible vasculature or defects, (c) cutting tool placed in the template hole, and (d) cutting performed by slowly rotating the cutting tool about the long axis to produce a cylindrical specimen

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Fig. 4

Experimental setup for the uniaxial compression tests

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Fig. 5

Exemplar top-view and side-view pretest photos taken to quantify the initial specimen area and height

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Fig. 6

Exemplar raw force versus time history illustrating the inflection point used to define the time of failure. The load increased again after the point of failure due to the fact that with continued compression, the load is redistributed throughout the sample.

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Fig. 7

Stress versus strain curves for human liver parenchyma specimens loaded at 0.01 s−1

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Fig. 8

Stress versus strain curves for human liver parenchyma specimens loaded at 0.10 s−1

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Fig. 9

Stress versus strain curves for human liver parenchyma specimens loaded at 1.00 s−1

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Fig. 10

Stress versus strain curves for human liver parenchyma specimens loaded at 10.0 s−1

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Fig. 11

Comparison of peak true stress for isolated samples of porcine, human, and bovine liver parenchyma loaded in compression

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Fig. 12

Comparison of peak nominal strain for isolated samples of porcine, human, and bovine liver parenchyma loaded in compression

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