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Influence of prenatal hypoxia and postnatal hyperoxia on morphologic lung maturation in mice
Andreas Schmiedl1,2,3, Torge Roolfs1, Erol Tutdibi4
1Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany.
Insights
Prenatal hypoxia combined with postnatal hyperoxia significantly hinders lung development in mice, leading to alterations resembling bronchopulmonary dysplasia (BPD). This combined exposure is crucial for modeling BPD-like lung changes.
Area of Science:
- Neonatal Medicine
- Developmental Biology
- Respiratory Physiology
Background:
- Oxygen therapy is vital for preterm infants but can impact lung development.
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease resulting from oxygen exposure and lung injury.
- Current experimental BPD models lack comparative studies on oxygen's influence on lung maturation.
Purpose of the Study:
- To investigate how prenatal hypoxia and postnatal hyperoxia affect lung maturation.
- To identify which experimental model best mimics BPD-related lung alterations using stereology.
Main Methods:
- Mice were exposed to normoxia or hypoxia prenatally.
- Offspring were exposed to normoxia or hyperoxia postnatally, creating four groups: No/No, No/Hyper, Hypo/No, Hypo/Hyper.
- Stereological analysis was performed on 14-day-old pups.
Main Results:
- Combined prenatal hypoxia and postnatal hyperoxia (Hypo/Hyper) significantly reduced lung volume and air space volume.
- The Hypo/Hyper group showed increased airspace size and septal wall thickness.
- Lamellar body volume in alveolar epithelial cells type II was significantly lower in the Hypo/Hyper group.
Conclusions:
- Prenatal hypoxia and postnatal hyperoxia have distinct effects on lung maturation.
- The combination of both exposures is necessary to induce significant BPD-like morphological changes in 14-day-old mice.
Background:
Oxygen supply as a lifesaving intervention is frequently used to treat preterm infants suffering additionally from possible prenatal or perinatal pathogen features. The impact of oxygen and/or physical lung injury may influence the morphological lung development, leading to a chronic postnatal lung disease called bronchopulmonary dysplasia (BPD). At present different experimental BPD models are used. However, there are no systematic comparative studies regarding different influences of oxygen on morphological lung maturation.
Objective:
We investigated the influence of prenatal hypoxia and/or postnatal hyperoxia on morphological lung maturation based on stereological parameters, to find out which model best reflects morphological changes in lung development comparable with alterations found in BPD.
Methods:
Pregnant mice were exposed to normoxia, the offspring to normoxia (No/No) or to hyperoxia (No/Hyper). Furthermore, pregnant mice were exposed to hypoxia and the offspring to normoxia (Hypo/No) or to hyperoxia (Hypo/Hyper). Stereological investigations were performed on all pups at 14 days after birth.
Results:
Compared to controls (No/No) 1) the lung volume was significantly reduced in the No/Hyper and Hypo/Hyper groups, 2) the volume weighted mean volume of the parenchymal airspaces was significantly higher in the Hypo/Hyper group, 3) the total air space volume was significantly lower in the No/Hyper and Hypo/Hyper groups, 4) the total septal surface showed significantly lower values in the No/Hyper and Hypo/Hyper groups, 5) the wall thickness of septa showed the highest values in the Hypo/Hyper group without reaching significance, 6) the volume density and the volume weighted mean volume of lamellar bodies in alveolar epithelial cells type II (AEII) were significantly lower in the Hypo/Hyper group.
Conclusion:
Prenatal hypoxia and postnatal hyperoxia differentially influence the maturation of lung parenchyma. In 14 day old mice a significant retardation of morphological lung development leading to BPD-like alterations indicated by different parameters was only seen after hypoxia and hyperoxia.
