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Structural multi-mechanism model with anisotropic damage for cerebral arterial tissues and its finite element modeling.

机译:具有各向异性损伤的脑动脉组织结构多机制模型及其有限元建模。

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摘要

A structural multi-mechanism constitutive equation is proposed to describe the anisotropic and damage behavior of cerebral arterial tissue. The arterial tissue is modeled as a non-linear, incompressible and inelastic material. In this model, new deformation criteria are proposed for the recruitment of collagen fibers and degradation of internal elastic lamina (IEL), two important features of early stage aneurysm formation. This structural anisotropic model is formulated by modifying a previous multi-mechanism model to include the fibrous nature of collagen fibers and incorporates morphological information such as fiber orientation and dispersion. An anisotropic damage model is included to characterize tissue weakening and softening before failure of the IEL, ground matrix or collagen fibers. Two possible damage mechanisms are formulated in this model: mechanical damage dependent on material strains and enzymatic damage induced by hemodynamic stresses.;The elastin/ground matrix and collagen fibers are treated as separate components of arteries. The elastin and ground matrix, which are represented by an isotropic response, bear loads at low strain level, and degrade gradually due to damage or disrupt due to eventual failure. The collagen fibers are recruited into load-bearing and subfailure damage at higher strain levels. Two approaches are considered for modeling their anisotropic behavior. In the first, they are characterized by the anisotropic behavior of N fibers. In the second, the collagen fibers are arranged in two helically oriented families with dispersion in their orientation. The fiber distribution is modeled by an orientation density function or distribution parameter. The fiber orientation and dispersion can be prescribed from arterial histology studies, or identified from stress-strain response as structural parameters.;Pressure inflation test data for cerebral arteries are used to evaluate the constitutive model. It is found to fit the mechanical response of uniaxial test well. There is a need for additional experimental data to further evaluate and develop this model. The constitutive model is implemented in commercial finite element analysis package for numerical computation. The numerical implementation is validated by analytical solutions. The numerical model is used for the study of arterial microstructural behavior in complex biomechanical procedure of angioplasty surgery.
机译:提出了一种结构多机理的本构方程来描述脑动脉组织的各向异性和损伤行为。动脉组织被建模为非线性,不可压缩和无弹性的材料。在该模型中,提出了新的变形标准,用于胶原纤维的募集和内部弹性层的降解(IEL),这是早期动脉瘤形成的两个重要特征。通过修改以前的多机制模型以包含胶原纤维的纤维性质,并结合诸如纤维取向和分散等形态信息,可以构造出这种结构各向异性模型。包括各向异性损伤模型以表征IEL,基质或胶原纤维失效前组织的软化和软化。在该模型中提出了两种可能的损伤机制:取决于材料应变的机械损伤和由血流动力学应力引起的酶促损伤。弹性蛋白/基质和胶原纤维被视为动脉的独立组成部分。用各向同性响应表示的弹性蛋白和地基在低应变水平下承受载荷,并由于损坏或最终失效而破坏而逐渐降解。在较高的应变水平下,胶原纤维被吸收到承重和亚破坏损伤中。考虑了两种方法来对它们的各向异性行为进行建模。首先,它们的特征在于N纤维的各向异性。在第二种方法中,胶原纤维排列成两个螺旋取向的家族,其取向分散。纤维分布通过定向密度函数或分布参数建模。纤维的取向和分散可以从动脉组织学研究中确定,或从应力-应变响应中识别为结构参数。;脑动脉的压力充气测试数据用于评估本构模型。发现它适合单轴测试的机械响应。需要其他实验数据来进一步评估和开发该模型。本构模型在商业有限元分析软件包中实现,用于数值计算。通过解析解验证了数值实现。该数值模型用于研究血管成形术复杂生物力学过程中的动脉微结构行为。

著录项

  • 作者

    Li, Dalong.;

  • 作者单位

    University of Pittsburgh.;

  • 授予单位 University of Pittsburgh.;
  • 学科 Engineering Biomedical.;Engineering Mechanical.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 117 p.
  • 总页数 117
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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