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    Effects of Pulmonary Fibrosis and Surface Tension on Alveolar Sac Mechanics in Diffuse Alveolar Damage

    Source: Journal of Biomechanical Engineering:;2021:;volume( 143 ):;issue: 008::page 081013-1
    Author:
    Chen, Long
    ,
    Tao, Weiwei
    ,
    Ji, Wei
    ,
    Lu, Yan
    ,
    Zhao, Xia
    DOI: 10.1115/1.4050789
    Publisher: The American Society of Mechanical Engineers (ASME)
    Abstract: Diffuse alveolar damage (DAD) is a characteristic histopathologic pattern in most cases of acute respiratory distress syndrome and severe viral pneumonia, such as COVID-19. DAD is characterized by an acute phase with edema, hyaline membranes, and inflammation followed by an organizing phase with pulmonary fibrosis and hyperplasia. The degree of pulmonary fibrosis and surface tension is different in the pathological stages of DAD. The effects of pulmonary fibrosis and surface tension on alveolar sac mechanics in DAD are investigated by using the fluid–structure interaction (FSI) method. The human pulmonary alveolus is idealized by a three-dimensional honeycomb-like geometry, with alveolar geometries approximated as closely packed 14-sided polygons. A dynamic compression-relaxation model for surface tension effects is adopted. Compared to a healthy model, DAD models are created by increasing the tissue thickness and decreasing the concentration of the surfactant. The FSI results show that pulmonary fibrosis is more influential than the surface tension on flow rate, volume, P–V loop, and resistance. The lungs of the disease models become stiffer than those of the healthy models. According to the P–V loop results, the surface tension plays a more important role in hysteresis than the material nonlinearity of the lung tissue. Our study demonstrates the differences in air flow and lung function on the alveolar sacs between the healthy and DAD models.
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      Effects of Pulmonary Fibrosis and Surface Tension on Alveolar Sac Mechanics in Diffuse Alveolar Damage

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    contributor authorChen, Long
    contributor authorTao, Weiwei
    contributor authorJi, Wei
    contributor authorLu, Yan
    contributor authorZhao, Xia
    date accessioned2022-02-06T05:30:06Z
    date available2022-02-06T05:30:06Z
    date copyright5/6/2021 12:00:00 AM
    date issued2021
    identifier issn0148-0731
    identifier otherbio_143_08_081013.pdf
    identifier urihttp://yetl.yabesh.ir/yetl1/handle/yetl/4278164
    description abstractDiffuse alveolar damage (DAD) is a characteristic histopathologic pattern in most cases of acute respiratory distress syndrome and severe viral pneumonia, such as COVID-19. DAD is characterized by an acute phase with edema, hyaline membranes, and inflammation followed by an organizing phase with pulmonary fibrosis and hyperplasia. The degree of pulmonary fibrosis and surface tension is different in the pathological stages of DAD. The effects of pulmonary fibrosis and surface tension on alveolar sac mechanics in DAD are investigated by using the fluid–structure interaction (FSI) method. The human pulmonary alveolus is idealized by a three-dimensional honeycomb-like geometry, with alveolar geometries approximated as closely packed 14-sided polygons. A dynamic compression-relaxation model for surface tension effects is adopted. Compared to a healthy model, DAD models are created by increasing the tissue thickness and decreasing the concentration of the surfactant. The FSI results show that pulmonary fibrosis is more influential than the surface tension on flow rate, volume, P–V loop, and resistance. The lungs of the disease models become stiffer than those of the healthy models. According to the P–V loop results, the surface tension plays a more important role in hysteresis than the material nonlinearity of the lung tissue. Our study demonstrates the differences in air flow and lung function on the alveolar sacs between the healthy and DAD models.
    publisherThe American Society of Mechanical Engineers (ASME)
    titleEffects of Pulmonary Fibrosis and Surface Tension on Alveolar Sac Mechanics in Diffuse Alveolar Damage
    typeJournal Paper
    journal volume143
    journal issue8
    journal titleJournal of Biomechanical Engineering
    identifier doi10.1115/1.4050789
    journal fristpage081013-1
    journal lastpage081013-7
    page7
    treeJournal of Biomechanical Engineering:;2021:;volume( 143 ):;issue: 008
    contenttypeFulltext
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