Role of pulmonary surfactant in the development and treatment of adult respiratory distress syndrome.

The goal of this article has been to examine the role of pulmonary surfactant system alterations in the development of ARDS, and the potential efficacy of surfactant replacement therapy in ARDS and ARDS-type injuries. Data from patients with ARDS and animal models with ARDS-type injuries clearly indicate the existence of a surfactant-deficient state. However, in contrast to neonatal RDS, this deficiency generally does not represent the primary pathogenic factor. The diversity of the disorders associated with ARDS has made it impossible to develop a single-animal model that can be used to test potential therapeutic measures. The ARDS animal models that have been developed are equally diverse, and represent the wide variations in severity and time-course seen clinically. Nevertheless, almost all of the lung injury models show indications of surfactant abnormality, which is caused mainly by biophysical inhibition of surfactant activity by the large amounts of proteinaceous edema found in the injured lungs. In some cases, this surfactant dysfunction is further compounded by a quantitative surfactant deficiency brought about by metabolic alterations of the type II pneumocytes. It is important to note that all of the lung injury models studied thus far have shown significant improvements in pulmonary mechanics and arterial oxygenation after treatment with exogenous surfactant. Such results are consistent with biophysical studies that suggest that increasing the effective surfactant concentration in the lung should mitigate the effects of both quantitative and functional surfactant deficiencies. Although animal studies suggest that surfactant replacement therapy might be efficacious in ARDS, there is a good deal of experimental work that still needs to be done.(ABSTRACT TRUNCATED AT 250 WORDS)