Strain-induced inflammation in pulmonary alveolar tissue due to mechanical ventilation.

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Title: Strain-induced inflammation in pulmonary alveolar tissue due to mechanical ventilation.
Authors: Aghasafari, Parya1, Bin M. Ibrahim, Israr1, Pidaparti, Ramana1 rmparti@uga.edu
Source: Biomechanics & Modeling in Mechanobiology. Aug2017, Vol. 16 Issue 4, p1103-1118. 16p.
Subjects: Inflammation, Artificial respiration, Fluid-structure interaction, Physiologic strain, Computer simulation
Abstract: Inflammation is the body's attempt at self-protection to remove harmful stimuli, including damaged cells, irritants, or pathogens and begin the healing process. In this study, strain-induced inflammation in pulmonary alveolar tissue under high tidal volume is investigated through a combination of an inflammation model and fluid structure interaction (FSI) analysis. A realistic three-dimensional organ model for alveolar sacs is built, and FSI is employed to evaluate strain distribution in alveolar tissue for different tidal volume (TV) values under the mechanical ventilation (MV) condition. The alveolar tissue is treated as a hyperelastic solid and provides the environment for the tissue constituents. The influence of different strain distributions resulting from different tidal volumes is investigated. It is observed that strain is highly distributed in the inlet area. In addition, strain versus time curves in different locations through the alveolar model reveals that middle layers in the alveolar region would undergo higher levels of strain during breathing under the MV condition. Three different types of strain distributions in the alveolar region from the FSI simulation are transferred to the CA model to study population dynamics of cell constituents under MV for different TVs; 200, 500 and 1000 mL, respectively. The CA model results suggests that strain distribution plays a significant role in population dynamics. An interplay between strain magnitude and distribution appears to influence healing capability. Results suggest that increasing TV leads to an exponential rise in tissue damage by inflammation. [ABSTRACT FROM AUTHOR]
Copyright of Biomechanics & Modeling in Mechanobiology is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Strain-induced inflammation in pulmonary alveolar tissue due to mechanical ventilation.
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  Data: <searchLink fieldCode="AR" term="%22Aghasafari%2C+Parya%22">Aghasafari, Parya</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Bin+M%2E+Ibrahim%2C+Israr%22">Bin M. Ibrahim, Israr</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Pidaparti%2C+Ramana%22">Pidaparti, Ramana</searchLink><relatesTo>1</relatesTo><i> rmparti@uga.edu</i>
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  Data: <searchLink fieldCode="JN" term="%22Biomechanics+%26+Modeling+in+Mechanobiology%22">Biomechanics & Modeling in Mechanobiology</searchLink>. Aug2017, Vol. 16 Issue 4, p1103-1118. 16p.
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  Data: <searchLink fieldCode="DE" term="%22Inflammation%22">Inflammation</searchLink><br /><searchLink fieldCode="DE" term="%22Artificial+respiration%22">Artificial respiration</searchLink><br /><searchLink fieldCode="DE" term="%22Fluid-structure+interaction%22">Fluid-structure interaction</searchLink><br /><searchLink fieldCode="DE" term="%22Physiologic+strain%22">Physiologic strain</searchLink><br /><searchLink fieldCode="DE" term="%22Computer+simulation%22">Computer simulation</searchLink>
– Name: Abstract
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  Data: Inflammation is the body's attempt at self-protection to remove harmful stimuli, including damaged cells, irritants, or pathogens and begin the healing process. In this study, strain-induced inflammation in pulmonary alveolar tissue under high tidal volume is investigated through a combination of an inflammation model and fluid structure interaction (FSI) analysis. A realistic three-dimensional organ model for alveolar sacs is built, and FSI is employed to evaluate strain distribution in alveolar tissue for different tidal volume (TV) values under the mechanical ventilation (MV) condition. The alveolar tissue is treated as a hyperelastic solid and provides the environment for the tissue constituents. The influence of different strain distributions resulting from different tidal volumes is investigated. It is observed that strain is highly distributed in the inlet area. In addition, strain versus time curves in different locations through the alveolar model reveals that middle layers in the alveolar region would undergo higher levels of strain during breathing under the MV condition. Three different types of strain distributions in the alveolar region from the FSI simulation are transferred to the CA model to study population dynamics of cell constituents under MV for different TVs; 200, 500 and 1000 mL, respectively. The CA model results suggests that strain distribution plays a significant role in population dynamics. An interplay between strain magnitude and distribution appears to influence healing capability. Results suggest that increasing TV leads to an exponential rise in tissue damage by inflammation. [ABSTRACT FROM AUTHOR]
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  Label:
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  Data: <i>Copyright of Biomechanics & Modeling in Mechanobiology is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1007/s10237-017-0879-5
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              Text: Aug2017
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