Piantadosi C A, Fracica P J, Duhaylongsod F G, Huang Y C, Welty-Wolf K E, Crapo J D, Young S L
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Appl Physiol (1985). 1995 May;78(5):1823-31. doi: 10.1152/jappl.1995.78.5.1823.
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% O2 for 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 O2 exposures, lungs were fixed and processed for electron microscopy. The cellular responses to O2 included 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 O2 exposure 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.
高氧导致的弥漫性肺损伤伴有肺顺应性降低和低氧血症，同时伴有内皮细胞层和肺泡上皮细胞层的破坏。由于在动物和人类中，弥漫性肺损伤时表面活性剂的功能和含量均会降低，因此在灵长类动物中使用无蛋白表面活性剂治疗后，评估了持续高氧期间损伤程度的变化。十只狒狒用100%氧气通气96小时，五只间歇给予人工表面活性剂（Exosurf）气雾剂。表面活性剂治疗效果的生理和生化测量结果发表在一篇配套论文中（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和S. L. Young。《应用生理学杂志》78: 1823 - 1829, 1995）。氧气暴露后，将肺固定并进行电子显微镜处理。细胞对氧气的反应包括上皮细胞和内皮细胞损伤、间质水肿和炎症。形态计量学用于定量氧气暴露期间用人工表面活性剂治疗的动物肺部的变化，并将其与未治疗的动物进行比较。表面活性剂减少了中性粒细胞的积聚，增加了成纤维细胞的增殖，并减少了I型上皮细胞体积的变化。接受表面活性剂治疗的动物还表现出内皮细胞完整性的更好保存。这些反应表明表面活性剂对肺部对高氧的反应有改善作用，包括防止上皮细胞和内皮细胞破坏。然而，在持续高氧暴露的接受表面活性剂治疗的肺中，仍存在明显的间质炎症和成纤维细胞增殖。
