A comparative study of mechanisms of surfactant inhibition
A comparative study of mechanisms of surfactant inhibition
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DOI：
10.1016/j.bbamem.2007.10.027
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发表时间：
2008-02-01
影响因子：
3.4
通讯作者：
Amrein, Matthias W.
中科院分区：
文献类型：
--
作者：
Gunasekara, Lasantha;Schoel, W. Michael;Amrein, Matthias W.
肺表面活性剂扩散到水合空气-肺界面，并将表面张力降低到非常小的值。在急性呼吸窘迫综合征（ARDS）中，该功能失效，表面张力保持高水平。功能障碍已被归因于血浆蛋白和表面活性剂之间的空气-肺界面的竞争，或者，表面活性剂的分子谱的ARDS特异性改变。在这里，我们在体外比较了这两种机制，以评估它们在引起呼吸窘迫中的潜在作用。白蛋白和纤维蛋白原暴露于血液水平浓度或高于血液水平浓度用作测试竞争性吸附的模型。选择胆固醇水平升高作为ARDS中表面活性剂分子谱的已知不利变化。将牛脂质提取物表面活性剂（BLES）从浓缩悬浮液的小团（27 mg/ml）铺展到捕获气泡表面活性计（CBS）中的空气-水界面，并且循环地减小和增加气泡体积以评估铺展材料的表面活性。选择抑制剂的浓度和肺表面活性物质的浓度和扩散方法，试图重现肺表面活性物质对抑制剂的暴露。在这些条件下，血清白蛋白和纤维蛋白原都没有持续抑制作用，并且在少量循环后获得了正常的接近零的最小表面张力值。相反，即使在广泛的循环后，胆固醇水平增加的抑制作用仍然存在。这些结果表明，在ARDS中，竞争性吸附可能不足以解释高表面张力，表面活性剂膜的破坏需要考虑因果关系。(c)2007 Elsevier B. V.保留所有权利。
Pulmonary surfactant spreads to the hydrated air-lung interface and reduces the surface tension to a very small value. This function fails in acute respiratory distress syndrome (ARDS) and the surface tension stays high. Dysfunction has been attributed to competition for the air-lung interface between plasma proteins and surfactant or, alternatively, to ARDS-specific alterations of the molecular profile of surfactant. Here, we compared the two mechanisms in vitro, to assess their potential role in causing respiratory distress. Albumin and fibrinogen exposure at or above blood level concentrations served as the models for testing competitive adsorption. An elevated level of cholesterol was chosen as a known adverse change in the molecular profile of surfactant in ARDS. Bovine lipid extract surfactant (BLES) was spread from a small bolus of a concentrated suspension (27 mg/ml) to the air-water interface in a captive bubble surfactometer (CBS) and the bubble volume was cyclically reduced and increased to assess surface activity of the spread material. Concentrations of inhibitors and the concentration and spreading method of pulmonary surfactant were chosen in an attempt to reproduce the exposure of surfactant to inhibitors in the lung. Under these conditions, neither serum albumin nor fibrinogen was persistently inhibitory and normal near-zero minimum surface tension values were obtained after a small number of cycles. In contrast, inhibition by an increased level of cholesterol persisted even after extensive cycling. These results suggest that in ARDS, competitive adsorption may not sufficiently explain high surface tension, and that disruption of the surfactant film needs to be given causal consideration. (c) 2007 Elsevier B.V. All rights reserved.