Creating a model of diseased artery damage and failure from healthy porcine aorta.
Creating a model of diseased artery damage and failure from healthy porcine aorta.
复制标题
利用健康的猪主动脉创建患病动脉损伤和衰竭的模型。
DOI:
10.1016/j.jmbbm.2016.02.018
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发表时间:
2016
影响因子:
3.9
通讯作者:
Z. Taylor
中科院分区:
文献类型:
--
作者:
Christopher Noble;Nicole Smulders;N. Green;R. Lewis;M. Carré;S. E. Franklin;S. MacNeil;Z. Taylor
Large quantities of diseased tissue are required in the research and development of new generations of medical devices, for example for use in physical testing. However, these are difficult to obtain. In contrast, porcine arteries are readily available as they are regarded as waste. Therefore, reliable means of creating from porcine tissue physical models of diseased human tissue that emulate well the associated mechanical changes would be valuable. To this end, we studied the effect on mechanical response of treating porcine thoracic aorta with collagenase, elastase and glutaraldehyde. The alterations in mechanical and failure properties were assessed via uniaxial tension testing. A constitutive model composed of the Gasser-Ogden-Holzapfel model, for elastic response, and a continuum damage model, for the failure, was also employed to provide a further basis for comparison (Calvo and Pena, 2006, Gasser et al., 2006). For the concentrations used here it was found that: collagenase treated samples showed decreased fracture stress in the axial direction only; elastase treated samples showed increased fracture stress in the circumferential direction only; and glutaraldehyde samples showed no change in either direction. With respect to the proposed constitutive model, both collagenase and elastase had a strong effect on the fibre-related terms. The model more closely captured the tissue response in the circumferential direction, due to the smoother and sharper transition from damage initiation to complete failure in this direction. Finally, comparison of the results with those of tensile tests on diseased tissues suggests that these treatments indeed provide a basis for creation of physical models of diseased arteries.
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影响因子:
2.4
作者:
Teng, Zhongzhao;Tang, Dalin;Zheng, Jie;Woodard, Pamela K.;Hoffman, Allen H.
通讯作者:
Hoffman, Allen H.
影响因子:
6.9
作者:
O'Connell, Mary K.;Murthy, Sushila;Taylor, Charles A.
通讯作者:
Taylor, Charles A.
DOI:
--
发表时间:
2012
期刊:
Molecular & cellular biomechanics : MCB
影响因子:
--
作者:
Martinez,Ricky;Han,Hai-Chao
通讯作者:
Han,Hai-Chao
DOI:
10.1152/ajpheart.00463.2011
发表时间:
2012-02-01
影响因子:
4.8
作者:
Lee, Avione Y.;Han, Boyang;Han, Hai-Chao
通讯作者:
Han, Hai-Chao
影响因子:
9.7
作者:
Kamenskiy, Alexey V.;Pipinos, Iraklis I.;MacTaggart, Jason N.
通讯作者:
MacTaggart, Jason N.