NATURAL SURFACTANT AND HYPEROXIC LUNG INJURY IN PRIMATES .1. PHYSIOLOGY AND BIOCHEMISTRY

Natural surfactant and hyperoxic lung injury in primates. I. Physiology and biochemistry. J. Appl. Physiol. 76(3): 991-1001, 1994. - 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 to hyperoxia. Twelve healthy male baboons (10-15 kg) were anesthetized, paralyzed, and mechanically ventilated with 2.5 cmH(2)O positive end-expiratory pressure (PEEP) for 96 h. Baboons were divided into three groups: 1) the O-2, group (n = 5) received 100% O-2, 2) the surfactant group (n = 5) received 100% O-2 and aerosolized porcine surfactant, and 3) a control group (n = 2) was ventilated at fractional concentration of inspired O-2 of 0.21 for 96 h to control for effects of anesthesia and mechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion (VA/Q) distribution was measured daily by multiple inert gas elimination technique. PEEP was increased once or twice daily to 10 cmH(2)O for 30 min to study its effects on measurements of VA/Q. At the end of experiments, lungs were obtained for biochemical analysis. Prolonged hyperoxia resulted in progressive worsening in VA/Q, hemodynamic deterioration, severe lung edema, and altered surfactant metabolism. Surfactant administration increased disaturated phosphatidylcholine in lavage fluid but did not improve lung edema or gas exchange. In the surfactant group, however, the addition of 10 cmH(2)O PEEP resulted in a greater degree of shunt reduction than did 2.5 cmH(2)O PEEP (47 vs. 31% in the O-2 group, P < 0.05). We conclude that aerosolized porcine surfactant did not prevent pulmonary O-2, injury in baboons, but it potentiated the shunt-reducing effect of PEEP.