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Published on: November 20, 2015
Delay in rat lung alveolarization after the combined exposure of maternal hyperglycemia and postnatal hyperoxia
Anna Koskinen1, Heikki Lukkarinen, Jukka Laine
1Research Centre of Applied and Preventive Cardiovascular Medicine (CAPC), University Hospital of Turku, Turku, Finland; Department of Paediatrics, University Hospital of Turku, Turku, Finland.
Insights
Maternal hyperglycemia alters fetal lung development. Postnatal oxygen exposure in neonatal rats with intrauterine hyperglycemia modifies lung growth, suggesting a protective effect against hyperoxia-induced damage.
Area of Science:
- Neonatal Physiology
- Developmental Biology
- Pulmonary Medicine
Background:
- Maternal diabetes negatively impacts fetal lung development.
- Postnatal treatments can further disrupt pulmonary growth in neonates.
Purpose of the Study:
- To investigate the impact of postnatal oxygen exposure on alveolar development.
- To examine neonatal rat lungs exposed to intrauterine hyperglycemia.
Main Methods:
- Diabetes induced in Sprague-Dawley rats via streptozotocin.
- Neonatal rats exposed to room air or 85% oxygen for 7 days.
- Lung analysis included weight, morphology, apoptosis, proliferation, and oxidative stress markers.
Main Results:
- Maternal hyperglycemia accelerated lung development (thinner alveolar walls, increased septation).
- Hyperoxia alone led to enlarged alveoli with few septa.
- Dual exposure inhibited alveolar wall thinning and delayed alveolar formation, altering apoptosis and proliferation.
Conclusions:
- Hyperglycemic priming modifies the detrimental effects of hyperoxia on neonatal rat alveolarization.
- This suggests a potential protective role of fetal hyperglycemia against hyperoxia-induced lung injury.
Background:
Maternal diabetes interferes with fetal lung development and postnatal treatments may further disturb pulmonary growth. Therefore, we investigated the effect of postnatal oxygen exposure on alveolar development in neonatal rat lungs pre-exposed to intrauterine hyperglycemia.
Methods:
Diabetes was induced in Sprague-Dawley rats with streptozotocin injection before pregnancy. Hyperglycemia-exposed and control litters were randomized to breath room air or 85% oxygen for 7 days after birth. Lungs were analyzed on postnatal d7 for weight, morphology, apoptosis, proliferation, and biomarkers of oxidative stress.
Results:
Maternal hyperglycemia accelerated lung development as demonstrated by thinner alveolar walls and slightly increased secondary septation when compared to room air bred rats. Hyperoxia alone caused thin-walled and enlarged alveoli with few secondary septa. Interestingly, the dual exposure inhibited the thinning of alveolar walls and the disappearance of mesenchymal cells from the alveolar walls together with the delay in the formation of alveoli and secondary crests. While the lungs' oxidative stress was similar in all groups, pulmonary apoptosis and proliferation were altered.
Conclusion:
Our results thus indicate that the hyperglycemic priming of the fetal lung modifies the deleterious effect of hyperoxia on alveolarization in neonatal rats.
