The biophysical function of pulmonary surfactant

Abstract

Pulmonary surfactant lowers surface tension in the lungs. Physiological studies indicate two key aspects of this function: that the surfactant film forms rapidly; and that when compressed by the shrinking alveolar area during exhalation, the film reduces surface tension to very low values. These observations suggest that surfactant vesicles adsorb quickly, and that during compression, the adsorbed film resists the tendency to collapse from the interface to form a three-dimensional bulk phase. Available evidence suggests that adsorption occurs by way of a rate-limiting structure that bridges the gap between the vesicle and the interface, and that the adsorbed film avoids collapse by undergoing a process of solidification. Current models, although incomplete, suggest mechanisms that would partially explain both rapid adsorption and resistance to collapse as well as how different constituents of pulmonary surfactant might affect its behavior.

Idiopathic Pulmonary Fibrosis May Be a Disease of Recurrent, Tractional Injury to the Periphery of the Aging Lung: A Unifying Hypothesis Regarding Etiology and Pathogenesis

“…Surfactant plays a critical role in preventing alveolar collapse at end-expiration and reduces alveolar surface tension during inspiration, thereby, increasing the mechanical efficiency of respiration. 57 Less than complete failure in these 2 functions might be survivable into adult life. Second, premature infants deficient in surfactant develop diffuse alveolar damage early after beginning respiration.…”

Compositional and structural characterization of monolayers and bilayers composed of native pulmonary surfactant from wild type mice

“…These different membranous structures represent key structural elements that are crucial to PulS function. This material contains 90% weight of phospholipids (saturated and unsaturated) and cholesterol, and 10% surfactant proteins (SP-) A, B, C and D. It is assumed that during the breathing cycles the low surface tension is achieved by an enrichment of PulS in saturated phospholipids (mainly DPPC), either by a selective DPPC inclusion, or by an exclusion of unsaturated phospholipids and cholesterol [2][3][4]. It has been shown that the particular composition of PulS causes lateral heterogeneities at the membrane plane.…”

“…It has been shown that the particular composition of PulS causes lateral heterogeneities at the membrane plane. For example, monolayers composed of representative surfactant lipids and organic lung surfactant extracts (from porcine or bovine sources) show densely packed segregated tilted liquid condensed (TLC) phase domains embedded in a liquid expanded (LE) phase, up to the so-called molecular squeeze-out or exclusion plateau [1][2][3][4][5]. Cholesterol dependent liquid immiscibility is also reported to be present in bilayers composed of native pulmonary surfactant at physiological temperatures [6].…”

Respiratory Care of the Neonate

“…A thin layer of a surfactant in the walls of the pulmonary alveoli at the end of each inspiration is not completely waterproof, some liquid passes through the pores being in contact with the air in the lung alveoli, increasing the surface tension and preventing the overdistension of the alveoli at the end of inspiration. The lung surfactant is rapidly adsorbed and easily distributed in the form of a thin film on the surface between the liquid layer and the air in the lung alveoli [32].…”