Effects of pulmonary oxygen injury on airway content of surfactant-associated protein A.

Abstract

The use of therapeutic hyperoxia has greatly improved the survival of infants born prematurely. However, high concentrations of oxygen cause pulmonary injury, leading to decreased pulmonary compliance and decreased oxygen diffusion. This injury can result in chronic pulmonary insufficiency. It has been hypothesized that the adverse effects of hyperoxia are mediated, in part, through changes in the pulmonary surfactant system. We investigated the effects of hyperoxia on surfactant-associated protein A (SP-A), the abundant surfactant-specific glycoprotein. Adult male rats were exposed to 85% oxygen for 72 h. Total lung volume and pulmonary compliance were measured, and alveolar surfactant material recovered by lavage. Hyperoxia decreased total lung capacity, and altered inflation and deflation hysteresis patterns. Disaturated phosphatidylcholine and SP-A content were significantly increased in alveolar surfactant material isolated from oxygen-treated rats. SP-A content was also significantly increased in lung tissue from oxygen-treated rats. The SP-A in the lavage of oxygen-treated rats appeared to be intact protein as no proteolytic fragments were detected and the SP-A migrated identically to that recovered from room air animals when analyzed by two-dimensional isoelectric focusing. We conclude that the decreased pulmonary compliance associated with pulmonary oxygen injury is not due to quantitative decreases in two major surfactant components, disaturated phosphatidylcholine and SP-A.