Literature DB >> 18511356

Biomechanics of liquid-epithelium interactions in pulmonary airways.

Samir N Ghadiali1, Donald P Gaver.   

Abstract

The delicate structure of the lung epithelium makes it susceptible to surface tension induced injury. For example, the cyclic reopening of collapsed and/or fluid-filled airways during the ventilation of injured lungs generates hydrodynamic forces that further damage the epithelium and exacerbate lung injury. The interactions responsible for epithelial injury during airway reopening are fundamentally multiscale, since air-liquid interfacial dynamics affect global lung mechanics, while surface tension forces operate at the molecular and cellular scales. This article will review the current state-of-knowledge regarding the effect of surface tension forces on (a) the mechanics of airway reopening and (b) epithelial cell injury. Due to the complex nature of the liquid-epithelium system, a combination of computational and experimental techniques are being used to elucidate the mechanisms of surface-tension induced lung injury. Continued research is leading to an integrated understanding of the biomechanical and biological interactions responsible for cellular injury during airway reopening. This information may lead to novel therapies that minimize ventilation induced lung injury.

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Year:  2008        PMID: 18511356      PMCID: PMC2652855          DOI: 10.1016/j.resp.2008.04.008

Source DB:  PubMed          Journal:  Respir Physiol Neurobiol        ISSN: 1569-9048            Impact factor:   1.931


  98 in total

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  44 in total

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4.  miR-146a regulates mechanotransduction and pressure-induced inflammation in small airway epithelium.

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Review 6.  Role of airway recruitment and derecruitment in lung injury.

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Review 7.  Liquid and surfactant delivery into pulmonary airways.

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Journal:  Respir Physiol Neurobiol       Date:  2008-05-23       Impact factor: 1.931

8.  A bioinspired microfluidic model of liquid plug-induced mechanical airway injury.

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9.  Hyperoxia increases the elastic modulus of alveolar epithelial cells through Rho kinase.

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