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肺泡内衬中与表面相关的表面活性剂储存库。

The surface-associated surfactant reservoir in the alveolar lining.

作者信息

Schürch S, Qanbar R, Bachofen H, Possmayer F

机构信息

Respiratory Research Group, Faculty of Medicine, University of Calgary, Canada.

出版信息

Biol Neonate. 1995;67 Suppl 1:61-76. doi: 10.1159/000244207.

DOI:10.1159/000244207
PMID:7647159
Abstract

A small atmospheric bubble was introduced into a surfactant suspension in a captive bubble surfactometer. After film formation to the equilibrium surface tension at the bubble air-liquid interface, the bulk phase surfactant was depleted by replacing the chamber contents several times with a saline-CaCl2 solution. The remaining film adsorbed at the bubble surface was then compressed stepwise in quasi-static fashion to near zero minimum surface tension. This was followed by a series of quasi-static expansion steps to surface tensions slightly above equilibrium. The surface tension of films from lipid extract surfactants and phospholipid mixtures did not increase in a manner consistent with the presence of a single surface monolayer. After the initial, rapid rise in surface tension at each expansion step, a decrease in surface tension to a new value was observed. This decrease in surface tension is likely due to the adsorption of 'surplus' material from a 'surface-associated reservoir' into the surface active film. The presence of surplus non-monolayer surfactant material in situ at the alveolar surface was also demonstrated by electron microscopy. SP-A acted as a potent promoter for the movement of excess material (equivalent to 2-3 monolayers) at the interface into the surface active film. In contrast, inhibitory serum proteins prevented the formation of a surface-associated reservoir or the adsorption of excess material into a surface active film.

摘要

将一个小的大气泡引入到俘获气泡表面张力仪中的表面活性剂悬浮液中。在气泡气液界面形成达到平衡表面张力的薄膜后,通过用盐水 - 氯化钙溶液多次替换腔室内容物来耗尽本体相中的表面活性剂。然后以准静态方式逐步压缩吸附在气泡表面的剩余薄膜,直至接近零最小表面张力。接着进行一系列准静态膨胀步骤,使表面张力略高于平衡值。脂质提取物表面活性剂和磷脂混合物形成的薄膜的表面张力增加方式与单一表面单层的存在不一致。在每个膨胀步骤中,表面张力最初快速上升之后,观察到表面张力下降到一个新值。表面张力的这种下降可能是由于“表面相关储存库”中的“多余”物质吸附到表面活性薄膜中。电子显微镜也证明了肺泡表面原位存在多余的非单层表面活性剂物质。表面活性蛋白A作为一种强效促进剂,促使界面处的过量物质(相当于2 - 3个单层)移动到表面活性薄膜中。相比之下,抑制性血清蛋白会阻止表面相关储存库的形成或过量物质吸附到表面活性薄膜中。

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