Letters to the Editor

The following are the abstracts of the articles discussed inthe subsequent letter:

  Huang, Yuh-Chin T., Aneysa C. Sane, Steven G. Simonson, Thomas A. Fawcett, Richard E. Moon,Philip J. Fracica, Margaret G. Menache, Claude A. Piantadosi, andStephen L. Young. Artificial surfactant attenuates hyperoxic lunginjury in primates. I. Physiology and biochemistry. J. Appl.Physiol. 78(5): 1816-1822, 1995.Prolonged exposure toO₂ causes diffuse alveolar damage and surfactantdysfunction that contribute to the pathophysiology of hyperoxic lunginjury. We hypothesized that exogenous surfactant would improve lungfunction during O₂ exposure in primates. Sixteen healthymale baboons (10-15 kg) were anesthetized and mechanically ventilated for 96 h. The animals received either 100% O₂(n = 6) or 100% O₂ plus aerosolized artificialsurfactant (Exosurf; n = 5). A third group of animals(n = 5) was ventilated with an inspired fraction ofO₂ of 0.21 to control for the effects of sedation andmechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion distribution(_A/) was measureddaily using a multiple inert-gas elimination technique. Positive end-expiratory pressure was kept at 2.5 cmH₂O andwas intermittently raised to 10 cmH₂O for 30 minto obtain additional measurements of_A/. After theexperiments, lungs were obtained for biochemical and histologicalassessment of injury. O₂ exposures altered hemodynamics,progressively worsened_A/, altered lung phospholipid composition, and produced severe lung edema. Artificial surfactant therapy significantly increased disaturatedphosphatidylcholine in lavage fluid and improved intrapulmonary shunt,arterial PO₂, and lung edema. Surfactant alsoenhanced the shunt-reducing effect of positive end-expiratory pressure.We conclude that an aerosolized protein-free surfactant decreased theprogression of pulmonary O₂ toxicity in baboons.