STUDY ON PATHOGENESIS OF RESPIRATORY FAILURE IN ACUTE LUNG INJURY

Abstract

Respiratory distress syndrome in the newborn resembles acute severe respiratory failure (ARF). ARF is associated with a number of ethiologies that cause diffuse lung injury. Hyperimmune rabbit serum against guinea pig lung proteins (ALS) induces acute fatal respiratory failure similar to ARF (Pädiatrie 14, 211,1975). We have studied movement of molecules in and out of the airways within 30 min after intravenous ALS. Guinea pigs that received saline or normal rabbit serum served as controls. 131I-Albumin and 14C, 3H-labeled surfactant were injected either intravenously or intratracheally prior to ALS. Following. ALS the airways became freely permeable to albumin. Despite effective mechanical ventilation the airways became flooded with protein. Within 30 min 26% (control 0.5%) of the intravenous 131I-albumin was recovered from the airways. More than 80% of intravenous surfactant was cleared from circulation but only 0.5% (control 0.02%) of it entered the airways. Lavageable surfactant pool decreased by 40% within 30 min after ALS. More than 95% of the complex that left the airways was recovered in the residual lung. Bronchial surfactant was inactivated by proteins and glycolipids that entered the airways after ALS. We have demonstrated a severe surfactant defect within 30 min after acute lung injury. We have also shown that the survival and lung function can be improved by surfactant substitution after ALS. Therefore we propose that surfactant deficiency plays a central role in early pathogenesis of ARF.