Neonatal hyperoxia alters the pulmonary alveolar and capillary structure of 40-day-old rats.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Randell, SH; Mercer, RR; Young, SL

Published Date

  • June 1990

Published In

Volume / Issue

  • 136 / 6

Start / End Page

  • 1259 - 1266

PubMed ID

  • 2356858

Pubmed Central ID

  • PMC1877590

International Standard Serial Number (ISSN)

  • 0002-9440


  • eng

Conference Location

  • United States