Background Oxidative stress may be important in the development of lung disease in the newborn. Immature, surfactant deficient lungs are particularly sensitive to damage from reactive oxygen species. Exogenous surfactant is the main treatment of respiratory distress syndrome (RDS). It replaces the endogenous surfactant pool and improves lung function, but also contributes important lung protective properties. Oxidative inactivation of exogenous surfactant may therefore increase susceptibility to ventilation-induced damage of the newborn lung.
Objective In an experimental animal model we tested the hypothesis that hyperoxia induces lipid peroxidation of exogenous surfactant with subsequent lung functional impairment.
Methods Surfactant deficient, preterm rabbits (n = 17) received intratracheal labeled surfactant (14C-DPPC-Curosurf) and were ventilated for 2 hours with either 100% oxygen or room air. Lung mechanics, bronchoalveolar lavage (BAL) and lung tissue were analyzed.
Results BAL from animals ventilated with 100% oxygen exhibited more lipid peroxidation (malondialdehyde) was compared to animals ventilated with room air. Dynamic compliance was lower and the tissue association, a measure of the ability of exogenous surfactant to enter endogenous metabolic pathways, was reduced (18% in 100% oxygen versus 34% in room air, p = 0.04).
Conclusion In an experimental model of RDS, ventilation with 100% oxygen induced inactivation of exogenous surfactant by lipid peroxidation and impaired lung function. This shows that avoiding hyperoxia after surfactant treatment is important for optimal treatment response. In the future, adding an anti-oxidant to the exogenous surfactant preparation may be a means to prevent inactivation and protect the immature lung from oxidation damage and subsequent adverse long-term respiratory outcome.
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