Biophysical behavior of lung surfactant: implications for respiratory physiology and pathophysiology

The major emphasis of this article has been the complex, multicomponent system of surfactants that are required for proper pulmonary mechanics and function in the mammalian lung. Although LS was discovered over 30 years ago, and soon after was linked directly with neonatal RDS, it has taken a significant time for researchers to develop a fundamental understanding of the pulmonary surfactant system, and its actions and roles in respiratory physiology. Nonetheless, knowledge about LS has increased greatly over the past decade, and it is now clear that exogenous surfactant replacement therapy for infants with RDS provides a substantial clinical advantage for these patients. Indeed, the therapy is life-saving in many very small premature infants, and as experience accrues, and therapy is optimized, this advance is clearly a major step forward in neonatology. Perhaps the most prominent theme that has been presented throughout the discussion here is that pulmonary surfactant research must take advantage of interdisciplinary descriptions and cross-correlations for accurate and rapid progress. One positive feature of prior work on lung surfactant replacement and RDS is that its difficulty has forced investigators toward a level of understanding that is sound enough to extend LS research into related fields, such as lung injury and ARDS. These areas have their own complications, including a much more diverse pathology and injury progressions than found with neonatal RDS. In fact, if defining the role of lung surfactant in ARDS (and developing replacement therapy for it) had been the goal of investigators before considering neonatal RDS, it is difficult to imagine a positive outcome. The situation now, however, is one where it is realistic to think of recognizing when and how LS effects will occur in different ARDS lung injuries, so that surfactant replacement will have the best opportunity to help mitigate their progressive pathology. In dealing with ARDS, it is well to remember that there are a variety of complicating factors, since lung injuries vary with animal age and species, and according to the level and duration of exposure. For example, in the hyperoxic injury described in the previous section there was clearly significant LS involvement. However, had animals been subjected to a lower level of oxygen (eg, 60%), even for a comparatively long time (eg, 21 days), the entire pathologic pattern would have been altered, as demonstrated, for example, by Holm et al.(ABSTRACT TRUNCATED AT 400 WORDS)