Pappas C T, Obara H, Bensch K G, Northway W H
Lab Invest. 1983 Jun;48(6):735-48.
Continuous exposure of newborn C57BL mice to 80% oxygen at normal atmospheric pressure for as many as 6 weeks results in significant pulmonary injury. This injury is reflected morphometrically and morphologically primarily in an increase in the pulmonary interstitial compartment and in pulmonary fibrosis. The fibrotic response is both peribronchiolar and parenchymal. Lowering the oxygen concentration of continuous exposure from 100 to 80% appears to reduce the cellular response of the alveolar lining cells and the bronchiolar mucosa in the newborn lung more than the fibrotic response. This suggests that the most persistent response in the growing lung to supplemental oxygen concentrations at or below 80% will be peribronchiolar and parenchymal fibrosis. These findings would account for the clinically observed reduction of stage II bronchopulmonary dysplasia, yet persistence of chronic bronchopulmonary dysplasia in human infants treated with supplemental oxygen concentrations below 100%.
将新生C57BL小鼠在正常大气压下持续暴露于80%氧气中长达6周会导致显著的肺损伤。这种损伤在形态计量学和形态学上主要表现为肺间质腔室增加和肺纤维化。纤维化反应既发生在细支气管周围，也发生在实质组织。将持续暴露的氧气浓度从100%降至80%似乎比纤维化反应更能减少新生肺中肺泡衬里细胞和细支气管黏膜的细胞反应。这表明，在生长中的肺中，对80%或更低的补充氧气浓度最持久的反应将是细支气管周围和实质组织纤维化。这些发现可以解释临床上观察到的II期支气管肺发育不良的减少，然而在接受低于100%补充氧气浓度治疗的人类婴儿中，慢性支气管肺发育不良仍然存在。
