Effect of Hyperoxia Exposure on Airway Beta-2-adrenergic Receptors

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Abstract RATIONALE Hyperoxia exposure causes harmful changes in developing lungs, resulting in pediatric lung diseases such as Bronchopulmonary Dysplasia. While the alveolar damage caused by hyperoxia is well-described, its effects on airways are less clear. This study investigated the impact of hyperoxia on airway composition and airflow regulators, such as pulmonary beta-2-adrenergic (B2) receptor and smooth muscle expression, in neonatal rats. METHODS Rat pups were randomized to control (FiO2 = 0.21) or hyperoxic (FiO2=0.9) conditions for the first 10 days of life (P1-P10). At P10, airflow was assessed using mean peak expiratory flow (PEF). PEF was measured via plethysmography prior to and 15 minutes following nebulization with either 90 mcg B2 receptor agonist Salbutamol (BA) or an equivalent volume of water (H2O). At P15, lungs were harvested for B2 receptor and smooth muscle actin protein expression quantification via Western blot. RESULTS At baseline, hyperoxia-exposed rat pups had significantly lower PEF than control rats (Control 3.23 mL/s vs Hyperoxia 2.56 mL/s, p = 0.02). Hyperoxia-exposed rat lungs expressed significantly more B2 receptor (Control 0.93 vs Hyperoxia 1.56, p=0.01) and smooth muscle actin (Control 0.94 vs Hyperoxia 3.05, p=0.0003) protein. There was no significant difference in percent PEF change following BA nebulization, relative to water nebulization (H2O-BA difference: Control 2% vs Hyperoxia 9%, p=0.99). CONCLUSION We found hyperoxia-exposure leads to impaired airflow and increased smooth muscle. Despite upregulated B2 receptor expression, hyperoxia exposed animals responded similarly to BA treatment. This suggests hyperoxia-associated airflow impairment may not be B2 receptor mediated.

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