Interfacial Phase Behavior of Pulmonary Surfactant

肺表面活性剂的界面相行为

基本信息

批准号：
6779061
负责人：
STEPHEN B HALL
金额：
$ 36.74万
依托单位：
OREGON HEALTH & SCIENCE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
1998
资助国家：
美国
起止时间：
1998-08-01 至 2006-07-31
项目状态：
已结题

项目摘要

DESCRIPTION (provided by applicant): This proposal concerns the mechanisms by which thin films of pulmonary surfactant form solid structures in the lungs. Surfactant films stabilize the small air spaces of the lungs by lowering the surface tension of the thin liquid layer that lines the alveoli. When compressed by the decreasing surface area during exhalation, the surfactant film reduces surface tension to extraordinarily low levels. In vitro, compressed monolayers containing the complete set of surfactant constituents fail to reach such low surface tensions because above an equilibrium density, constituents collapse from the interface. The ability of the two dimensional films to flow into the third dimension indicates fluid behavior. In the lungs, the persistence of the surfactant films at the interface when compressed to densities well above equilibrium indicates a solid structure. The classical model of surfactant function contends that only a film in the highly ordered tilted-condensed (TC) phase can be compressed to the low surface tensions observed in the lungs. Of the components in lung surfactant, only its most prevalent constituent, dipalmitoyl phosphatidylcholine (DPPC), can form the TC phase at physiological temperatures. Therefore the classical model explains the transformation of the surfactant film from fluid to solid structures in terms of a change in composition, with elimination of constituents other than DPPC, and a consequent transition between equilibrium phases. Our recently published and preliminary unpublished data, however, disagree with the predictions of the classical model. Our results suggest instead that the fluid surfactant films transform to solid structures by a process analogous to the supercooling of three dimensional liquids to form glass. The experiments proposed here will test first if fluid films transformed to solid structures by supercompression in vitro replicate the behavior of pulmonary surfactant in physiological settings, and then the extent to which the supercompressed fluid monolayers fit predictions of the analogy with supercooled liquids.

描述（由申请人提供）：该建议涉及肺表面活性剂薄膜形成肺部固体结构的机制。表面活性剂膜通过降低肺泡薄液层的表面张力来稳定肺的小空间。当呼气过程中的表面积减少压缩时，表面活性剂膜将表面张力降低至非常低的水平。在体外，包含完整表面活性剂成分组的压缩单层无法达到如此低的表面张力，因为高于平衡密度，成分从界面崩溃。两个维膜流入第三维的能力表明流体行为。在肺中，当压缩到高于平衡的密度时，表面活性剂膜在界面处的持久性表示固体结构。表面活性剂功能的经典模型认为，只有高度有序的倾斜度（TC）相中的膜才能压缩到肺中观察到的低表面张力。在肺表面活性剂中的成分中，只有其最普遍的成分二氨酰磷脂酰胆碱（DPPC）才能在生理温度下形成TC相。因此，经典模型解释了表面活性剂膜从流体到固体结构的转化，从而消除了除DPPC以外的其他成分，以及在平衡阶段之间的过渡。但是，我们最近发表的和初步未发表的数据不同意经典模型的预测。相反，我们的结果表明，流体表面活性剂膜通过类似于三维液体过冷的过程将其变成固体结构。如果在体外超压缩转化为固体结构的情况下，此处提出的实验将首先测试，从而在生理环境中复制了肺表面活性剂的行为，然后将超压缩流体单层拟合与超冷液体的类比的预测拟合的程度。