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Computational modeling of cell injury during pulmonary microbubble flows.

机译：肺微泡流动过程中细胞损伤的计算模型。

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摘要

Acute respiratory distress syndrome (ARDS) is a devastating cascade of deteriorating lung function characterized by fluid accumulation in the distal airways of the deep lung. During breathing, micron-sized bubbles of air propagate through these occluded airways, exerting abnormally-high hydrodynamic stresses on the cells that line the airway walls. The objective of this dissertation was to investigate the mechanical response of the cells to these injurious stresses through computational fluid-structure interaction models. Morphologically-accurate, 3D finite element models of alveolar epithelial cells were reconstructed from confocal microscopy images. Hydrodynamic stresses were calculated using the boundary element method. Results indicated that morphology has a significant influence on the risk of cell injury, with subconfluent cells developing higher membrane strains than confluent cells. Also, stiffening the cell membrane may have a protective effect on cells and this effect is more significant for confluent cells than subconfluent cells. To capture transient dynamic effects, a novel Prony-Dirichlet series constitutive formulation was developed for the soft glassy rheology (SGR) of cells, which is characterized by a weak power-law relationship between the complex shear modulus and frequency. The SGR model was used to show that maximum pressure gradient during airway reopening, not stress exposure duration, is responsible for cell injury as a consequence of the cells' soft glassy rheology properties. Furthermore, cell fluidization may mitigate cell injury. The SGR material formulation was extended to capture recently-reported timescale-dependent cell mechanics and results indicated that variations in the apparent power-law may arise from changes in the effective elasticity of the whole-cell cytoskeletal network. Finally, a finite element model of the oscillating optical tweezers microrheology technique showed that membrane mechanics contributions can increase apparent cell stiffness by up to two orders of magnitude. The modeling results were shown to be useful as a tool for suggesting future experimental studies of the effect of pharmacological agents on the risk of cell injury during ARDS. Advances in therapeutic treatments may lead to a reduction in ARDS-associated mortality and improved patient care.
机译：急性呼吸窘迫综合征（ARDS）是一种破坏性肺功能恶化级联，其特征是深部肺的远端气道中积聚了液体。在呼吸过程中，微米级的气泡通过这些被阻塞的气道传播，从而对沿气道壁排列的细胞施加异常高的流体动力应力。本文的目的是通过计算流体-结构相互作用模型研究细胞对这些有害应力的机械反应。从共聚焦显微镜图像重建了形态学精确的3D肺泡上皮细胞有限元模型。使用边界元法计算流体动力应力。结果表明形态对细胞损伤的风险有重大影响，亚融合细胞比融合细胞产生更高的膜菌株。而且，使细胞膜变硬可能对细胞具有保护作用，并且对于融合细胞而言，这种作用比亚融合细胞更为显着。为了捕获瞬态动力效应，开发了一种新颖的Prony-Dirichlet系列本构配方，用于细胞的软玻璃流变学（SGR），其特征在于复数剪切模量和频率之间的幂律关系较弱。 SGR模型用于显示气道重新开放过程中的最大压力梯度，而不是应力暴露持续时间，是由于细胞柔软的玻璃状流变特性导致细胞损伤的原因。此外，细胞流化可以减轻细胞损伤。 SGR材料的配方扩展到捕获最近报告的时间尺度依赖的细胞力学，结果表明，表观幂律的变化可能是由于全细胞细胞骨架网络的有效弹性的变化引起的。最后，振荡光镊微流变技术的有限元模型表明，膜力学的作用可以使表观细胞刚度增加多达两个数量级。结果表明，建模结果可作为一种工具，用于建议对ARDS期间药理剂对细胞损伤风险的影响进行未来的实验研究。治疗方法的进步可能会导致ARDS相关死亡率降低，并改善患者护理。

著录项

  • 作者

    Dailey, Hannah L.;

  • 作者单位

    Lehigh University.;

  • 授予单位 Lehigh University.;
  • 学科 Engineering Biomedical.;Engineering Mechanical.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 206 p.
  • 总页数 206
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物医学工程;机械、仪表工业;
  • 关键词

  • 入库时间 2022-08-17 11:38:25

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