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炎症产物对扩张力学的影响可引发拉普拉斯不稳定性和急性呼吸窘迫综合征。

Inflammation product effects on dilatational mechanics can trigger the Laplace instability and acute respiratory distress syndrome.

作者信息

Barman Sourav, Davidson Michael L, Walker Lynn M, Anna Shelly L, Zasadzinski Joseph A

机构信息

Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, Minnesota, USA.

Department of Chemical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.

出版信息

Soft Matter. 2020 Jul 29;16(29):6890-6901. doi: 10.1039/d0sm00415d.

DOI:10.1039/d0sm00415d
PMID:32643749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7462632/
Abstract

In the lungs, the Laplace pressure, ΔP = 2γ/R, would be higher in smaller alveoli than larger alveoli unless the surface tension, γ decreases with alveolar interfacial area, A, such that 2ε > γ in which ε = A(dγ/dA) is the dilatational modulus. In Acute Respiratory Distress Syndrome (ARDS), lipase activity due to the immune response to an underlying trauma or disease causes single chain lysolipid concentrations to increase in the alveolar fluids via hydrolysis of double-chain phospholpids in bacterial, viral, and normal cell membranes. Increasing lysolipid concentrations decrease the dilatational modulus dramatically at breathing frequencies if the soluble lysolipid has sufficient time to diffuse off the interface, causing 2ε < γ, thereby potentially inducing the "Laplace Instability", in which larger alveoli have a lower internal pressure than smaller alveoli. This can lead to uneven lung inflation, alveolar flooding, and poor gas exchange, typical symptoms of ARDS. While the ARDS lung contains a number of lipid and protein species in the alveolar fluid in addition to lysolipids, the surface activity and frequency dependent dilatational modulus of lysolipid suggest how inflammation may lead to the lung instabilities associated with ARDS. At high frequencies, even at high lysolipid concentrations, 2ε - γ > 0, which may explain the benefits ARDS patients receive from high frequency oscillatory ventilation.

摘要

在肺部,拉普拉斯压力ΔP = 2γ/R,在较小肺泡中会比在较大肺泡中更高,除非表面张力γ随肺泡界面面积A减小,使得2ε > γ,其中ε = A(dγ/dA)是膨胀模量。在急性呼吸窘迫综合征(ARDS)中,对潜在创伤或疾病的免疫反应导致的脂肪酶活性,通过细菌、病毒和正常细胞膜中双链磷脂的水解,使肺泡液中单链溶血脂质浓度增加。如果可溶性溶血脂质有足够时间从界面扩散离开,在呼吸频率下增加的溶血脂质浓度会显著降低膨胀模量,导致2ε < γ,从而可能引发“拉普拉斯不稳定”,即较大肺泡的内部压力低于较小肺泡。这会导致肺部充气不均匀、肺泡积水和气体交换不良,这是ARDS的典型症状。虽然ARDS肺的肺泡液中除了溶血脂质外还含有多种脂质和蛋白质,但溶血脂质的表面活性和频率依赖性膨胀模量表明炎症可能如何导致与ARDS相关的肺部不稳定。在高频时,即使在高溶血脂质浓度下,2ε - γ > 0,这可能解释了ARDS患者从高频振荡通气中获得的益处。

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