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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
Published on: October 19, 2013
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Airway Hyperreactivity Is Delayed after Mild Neonatal Hyperoxic Exposure.
Harris Onugha1, Peter M MacFarlane, Catherine A Mayer
1Division of Neonatology, Rainbow Babies and Children's Hospital, and Department of Pediatrics, Case Western Reserve University, Cleveland, Ohio, USA.
Neonatology
|May 30, 2015
Summary
Neonatal exposure to mild hyperoxia delayed airway hyperreactivity in mice, suggesting long-term changes in airway smooth muscle development. This may explain wheezing disorders in infants after premature birth.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Developmental biology
Background:
- Wheezing disorders are common in infants born prematurely.
- Neonatal hyperoxia is a risk factor for respiratory issues in these infants.
Purpose of the Study:
- To investigate the long-term effects of neonatal hyperoxia on airway hyperreactivity.
- To determine the impact of mild (40% oxygen) versus severe (70% oxygen) hyperoxia.
Main Methods:
- A neonatal mouse model was used to assess airway reactivity.
- In vitro living lung slice preparation was employed at postnatal days 8 and 21.
- Measurements included airway reactivity, smooth muscle actin, myosin light chain (MLC), and alveolar morphology.
Main Results:
- No immediate changes in airway reactivity were observed at postnatal day 8.
- Mild hyperoxia exposure led to enhanced airway reactivity at postnatal day 21, two weeks after exposure cessation.
- Increased airway alpha-smooth muscle actin expression was noted after mild hyperoxia, without significant MLC changes.
- Both mild and severe hyperoxia reduced alveolar counts at both time points.
Conclusions:
- Early, mild neonatal hyperoxia exposure results in a delayed increase in airway reactivity.
- This suggests a long-term alteration in airway smooth muscle development.
- Findings align with the persistent symptomatology observed in former preterm infants.
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