Letters to the Editor

Abstract

The following are the abstracts of the articles discussed in the 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, and Stephen L. Young. Artificial surfactant attenuates hyperoxic lung injury in primates. I. Physiology and biochemistry. J. Appl. Physiol. 78(5): 1816–1822, 1995.—Prolonged exposure to O2causes diffuse alveolar damage and surfactant dysfunction that contribute to the pathophysiology of hyperoxic lung injury. We hypothesized that exogenous surfactant would improve lung function during O2exposure in primates. Sixteen healthy male baboons (10–15 kg) were anesthetized and mechanically ventilated for 96 h. The animals received either 100% O2( n = 6) or 100% O2plus aerosolized artificial surfactant (Exosurf; n = 5). A third group of animals ( n = 5) was ventilated with an inspired fraction of O2of 0.21 to control for the effects of sedation and mechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion distribution (V˙A/Q˙) was measured daily using a multiple inert-gas elimination technique. Positive end-expiratory pressure was kept at 2.5 cmH2O and was intermittently raised to 10 cmH2O for 30 min to obtain additional measurements ofV˙A/Q˙. After the experiments, lungs were obtained for biochemical and histological assessment of injury. O2exposures altered hemodynamics, progressively worsenedV˙A/Q˙, altered lung phospholipid composition, and produced severe lung edema. Artificial surfactant therapy significantly increased disaturated phosphatidylcholine in lavage fluid and improved intrapulmonary shunt, arterial Po2, and lung edema. Surfactant also enhanced the shunt-reducing effect of positive end-expiratory pressure. We conclude that an aerosolized protein-free surfactant decreased the progression of pulmonary O2toxicity in baboons.Piantadosi, Claude A., Philip J. Fracica, Francis G. Duhaylongsod, Y.-C. T. Huang, Karen E. Welty-Wolf, James D. Crapo, and Stephen L. Young. Artificial surfactant attenuates hyperoxic lung injury in primates. II. Morphometric analysis. J. Appl. Physiol. 78(5): 1823–1831, 1995.—Diffuse lung injury from hyperoxia is accompanied by low compliance and hypoxemia with disruption of endothelial and alveolar epithelial cell layers. Because both function and content of surfactant in diffuse lung injury decrease in animals and in humans, changes in the extent of injury during continuous hyperoxia were evaluated after treatments with a protein-free surfactant in primates. Ten baboons were ventilated with 100% O2for 96 h and five were intermittently given an aerosol of an artificial surfactant (Exosurf). Physiological and biochemical measurements of the effects of the surfactant treatment are presented in a companion paper (Y.-C. T. Huang, A. C. Sane, S. G. Simonson, T. A. Fawcett, R. E. Moon, P. J. Fracica, M. G. Menache, C. A. Piantadosi, and S. L. Young. J. Appl. Physiol. 78: 1823–1829, 1995.) After O2exposures, lungs were fixed and processed for electron microscopy. The cellular responses to O2included epithelial and endothelial cell injuries, interstitial edema, and inflammation. Morphometry was used to quantitate changes in lungs of animals treated with the artificial surfactant during O2exposure and to compare them with the untreated animals. The surfactant decreased neutrophil accumulation, increased fibroblast proliferation, and decreased changes in the volume of type I epithelial cells. Surfactant-treated animals also demonstrated better preservation of endothelial cell integrity. These responses indicate ameliorating effects of the surfactant on the pulmonary response to hyperoxia, including protection against epithelial and endothelial cell destruction. Significant interstitial inflammation and fibroblast proliferation remained, however, in surfactant-treated lungs exposed to continuous hyperoxia.