The micromechanics of lung alveoli: structure and function of surfactant and tissue components.

The micromechanics of lung alveoli: structure and function of surfactant and tissue components.
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肺肺泡的微力学:表面活性剂和组织成分的结构和功能。

DOI:
10.1007/s00418-018-1747-9
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发表时间:
2018-12
影响因子:
2.3
通讯作者:
Ochs M
Ochs M
中科院分区:
生物学3区
文献类型:
--
作者:
Knudsen L;Ochs M

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哺乳动物肺的结构设计经过优化,以发挥其主要功能:气体交换。它发生在肺泡区域(实质),空气和血液在大表面上紧密接触。空气通过传导气道树到达肺泡腔。血液在嵌入肺泡间隔的毛细血管网中流动。空气和血液之间的屏障由连续的肺泡上皮(I型和II型肺泡上皮细胞的镶嵌体)、连续的毛细血管内皮和其间的结缔组织层组成。凭借其呼吸运动,肺必须在整个生命中承受机械挑战。肺泡必须受到保护,以免过度膨胀,以及从崩溃的内在稳定因素。薄壁组织的机械稳定性由两个组成部分确保:结缔组织纤维网络和表面活性剂系统。结缔组织纤维形成由轴向纤维、外周纤维和间隔纤维组成的连续张力整体性(张力+完整性)骨干。表面活性剂(表面活性剂)是II型肺泡上皮细胞的分泌产物,并作为生物活性的连续薄膜覆盖肺泡上皮。在这里,我们简要回顾了与气体交换相关的结构组件。然后我们描述了我们目前对这些成分在正常条件下如何发挥作用以及肺损伤如何导致肺泡微观力学功能障碍最终导致肺纤维化的理解。
The mammalian lung´s structural design is optimized to serve its main function: gas exchange. It takes place in the alveolar region (parenchyma) where air and blood are brought in close proximity over a large surface. Air reaches the alveolar lumen via a conducting airway tree. Blood flows in a capillary network embedded in inter-alveolar septa. The barrier between air and blood consists of a continuous alveolar epithelium (a mosaic of type I and type II alveolar epithelial cells), a continuous capillary endothelium and the connective tissue layer in-between. By virtue of its respiratory movements, the lung has to withstand mechanical challenges throughout life. Alveoli must be protected from over-distension as well as from collapse by inherent stabilizing factors. The mechanical stability of the parenchyma is ensured by two components: a connective tissue fiber network and the surfactant system. The connective tissue fibers form a continuous tensegrity (tension + integrity) backbone consisting of axial, peripheral and septal fibers. Surfactant (surface active agent) is the secretory product of type II alveolar epithelial cells and covers the alveolar epithelium as a biophysically active thin and continuous film. Here, we briefly review the structural components relevant for gas exchange. Then we describe our current understanding of how these components function under normal conditions and how lung injury results in dysfunction of alveolar micromechanics finally leading to lung fibrosis.
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