The forces that act to resist distension include elastic resistance and the surface tension that is exerted by fluid in the alveoli. The lungs both secrete and absorb fluid in two antagonistic processes that normally leave only a very thin film of fluid on the alveolar surface. Fluid absorption is driven (through osmosis) by the active transport of Na+, while fluid secretion is driven by the active transport of Cl- out of the alveolar epithelial cells. Research has demonstrated that people with cystic fibrosis have a genetic defect in one of the Cl- carriers (called the cystic fibrosis transmembrane regulator, or CFTR, as described in chapter 6). This results in an imbalance of fluid absorption and secretion, so that the airway fluid becomes excessively viscous (with a lower water content) and difficult to clear.
The thin film of fluid normally present in the alveolus has a surface tension, which is due to the fact that water molecules at the surface are attracted more to other water molecules than to air. As a result, the surface water molecules are pulled tightly together by attractive forces from underneath. This surface tension produces a force that is directed inward, raising the pressure within the alveolus. As described by the law of Laplace, the pressure thus created is directly proportional to the surface tension and in versely proportional to the radius of the alveolus (fig. 16.11). According to this law, the pressure in a smaller alveolus would be greater than in a larger alveolus if the surface tension were the same in both. The greater pressure of the smaller alveolus would then cause it to empty its air into the larger one. This does not normally occur because, as an alveolus decreases in size, its surface tension (the numerator in the equation) is decreased at the same time that its radius (the denominator) is reduced. The reason for the decreased surface tension, which prevents the alveoli from collapsing, is described in the next section.
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