Surfactant abnormality after endotoxin-induced lung injury in guinea-pigs.

Endotoxin (30 mg/kg) or saline was given endotracheally to guinea-pigs in order to investigate surfactant function in respiratory failure. Six hours later, bronchoalveolar lavage was performed. The lavage was analyzed for protein, phospholipids and surface activity, and fractioned into the phospholipid-rich sediment and the phospholipid-poor supernatant. The latter fraction was analyzed for surfactant inhibitor activity. After endotoxin, PaO2 and static lung-thorax compliance decreased. The lavage from endotoxin-treated animals revealed a 180% increase in protein, a 52 67% decrease in surfactant phospholipids, and increased minimum surface tension, as compared to the controls. After endotoxin, the supernatant contained a 58% higher activity of surfactant inhibitor, and the sediment had slower surface adsorption than after saline. We propose that abnormal surfactant function is important in the pathogenesis of respiratory failure in high-permeability pulmonary edema.