ARTIFICIAL SURFACTANT ATTENUATES HYPEROXIC LUNG INJURY IN PRIMATES .1. PHYSIOLOGY AND BIOCHEMISTRY

Prolonged exposure to O-2 causes diffuse alveolar damage and surfactan t dysfunction that contribute to the pathophysiology of hyperoxic lung injury. We hypothesized that exogenous surfactant would improve lung function during O-2 exposure in primates. Sixteen healthy male baboons (10-15 kg) were anesthetized and mechanically ventilated for 96 h. Th e animals received either 100% O-2 (n = 6) or 100% O-2 plus aerosolize d artificial surfactant (Exosurf; n = 5). A third group of animals (n = 5) was ventilated with an inspired fraction of O-2 of 0.21 to contro l for the effects of sedation and mechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion distrib ution (V-A/Q) was measured daily using a multiple inert-gas eliminatio n technique. Positive end-expiratory pressure was kept at 2.5 cmH(2)O and was intermittently raised to 10 cmH(2)O for 30 min to obtain addit ional measurements of V-A/Q After the experiments, lungs were obtained for biochemical and histological assessment of injury. O-2 exposures altered hemodynamics, progressively worsened V-A/Q, altered lung phosp holipid composition, and produced severe lung edema. Artificial surfac tant therapy significantly increased disaturated phosphatidylcholine i n lavage fluid and improved intrapulmonary shunt, arterial PO2, and lu ng edema. Surfactant also enhanced the shunt-reducing effect of positi ve end-expiratory pressure. We conclude that an aerosolized protein-fr ee surfactant decreased the progression of pulmonary O-2 toxicity in b aboons.