Randell S H, Mercer R R, Young S L
Department of Medicine, Durham Veterans Affairs Medical Center, North Carolina.
Am J Pathol. 1990 Jun;136(6):1259-66.
High inspired oxygen concentrations during the neonatal period profoundly inhibit rat lung development, an effect that is partly reversed during recovery in air. Persistent effects of neonatal hyperoxia on the size and number of alveoli or the structure of pulmonary capillaries have not been well defined. Using light and electron microscopic morphometry plus quantitative three-dimensional reconstructions of alveoli, we examined the lungs of 40-day-old rats that were exposed to more than 95% oxygen for the first 7 days after birth. Neonatal hyperoxia administered to rats resulted in abnormally enlarged air spaces at age 40 days. The fraction of the lung consisting of parenchyma was significantly increased and alveolar surface area was 13% lower than controls. There was an abnormal enlargement of alveolar ducts, which reduced by 24% the relative amount of air in the alveoli, compared to that in the alveolar ducts. The number of alveoli per lung and the mean volume of an alveolus were not different between the groups, but alveolar size class distributions were different, with significantly more very small and very large alveoli in 40-day-old rats after neonatal hyperoxia. By scanning electron microscopy, the alveolar surface of the exposed animals had a corrugated appearance, which was especially evident along alveolar ducts. Transmission electron microscopy revealed a greater density of capillaries, particularly in the alveolar regions close to terminal airways. Based on a random sample of the entire parenchymal region, capillary blood volume per cm2 of alveolar basal lamina was 18% greater. The results demonstrate that neonatal exposure to hyperoxia can cause abnormalities in the pulmonary alveolar and capillary structure of 40-day-old rats, and that these changes are similar to some features of broncho-pulmonary dysplasia.
新生儿期高吸入氧浓度会严重抑制大鼠肺发育,这种影响在恢复至空气中时会部分逆转。新生儿高氧对肺泡大小和数量或肺毛细血管结构的持续影响尚未明确界定。我们使用光镜和电镜形态计量学以及肺泡的定量三维重建技术,检查了出生后前7天暴露于95%以上氧气的40日龄大鼠的肺。对大鼠给予新生儿高氧会导致40日龄时气腔异常增大。肺实质所占比例显著增加,肺泡表面积比对照组低13%。肺泡管异常增大,与肺泡管相比,肺泡内空气的相对量减少了24%。两组之间每肺肺泡数量和单个肺泡平均体积无差异,但肺泡大小分类分布不同,新生儿高氧后的40日龄大鼠中非常小和非常大的肺泡明显更多。通过扫描电子显微镜观察,暴露动物的肺泡表面呈波纹状,沿肺泡管尤为明显。透射电子显微镜显示毛细血管密度更高,特别是在靠近终末气道的肺泡区域。基于整个实质区域的随机样本,每平方厘米肺泡基膜的毛细血管血容量增加了18%。结果表明,新生儿暴露于高氧可导致40日龄大鼠肺泡和毛细血管结构异常,且这些变化类似于支气管肺发育不良的一些特征。