Natural surfactant and hyperoxic lung injury in primates. I. Physiology and biochemistry

摘要: Surfactant dysfunction contributes to the pathophysiology of adult respiratory distress syndrome (ARDS), and we hypothesized that surfactant treatment would improve experimental ARDS produced by continuous exposure hyperoxia. Twelve healthy male baboons (10-15 kg) were anesthetized, paralyzed, mechanically ventilated with 2.5 cmH2O positive end-expiratory pressure (PEEP) for 96 h. Baboons divided into three groups: 1) O2 group (n = 5) received 100% O2, 2) aerosolized porcine surfactant, 3) a control was at fractional concentration inspired 0.21 h effects anesthesia mechanical ventilation. Hemodynamic parameters obtained every 12 h, ventilation-perfusion (VA/Q) distribution measured daily multiple inert gas elimination technique. PEEP increased once or twice 10 30 min study its on measurements VA/Q. At end experiments, lungs biochemical analysis. Prolonged hyperoxia resulted in progressive worsening VA/Q, hemodynamic deterioration, severe lung edema, altered metabolism. administration disaturated phosphatidylcholine lavage fluid but did not edema exchange. In group, however, addition greater degree shunt reduction than (47 vs. 31% P < 0.05). We conclude prevent pulmonary injury baboons, it potentiated shunt-reducing effect PEEP.