A review of the effects of early postnatal hyperoxia exposure on the immature brain.

Preterm birth is a public health priority worldwide, with approximately 15 million premature babies born each year. Oxygen supplementation is one of the most common interventions for preterm infants. However, prolonged oxygen inhalation at supraphysiological concentrations can lead to the development of bronchopulmonary dysplasia (BPD). In addition to lifelong pulmonary sequelae, clinical evidence suggests that BPD is associated with adverse neurodevelopmental outcomes, such as motor impairment, cognitive impairment, and behavioral deficits, severely affecting the quality of life of preterm infants. However, the mechanisms underlying the combination of neurodevelopmental impairment with BPD remain unclear. Therefore, in recent years, attention has also been focused on the effects of hyperoxia on brain development in preterm infants. In this review, we outline the pathophysiological mechanisms of brain injury caused by developmental hyperoxia exposure in current animal models and briefly describe the pharmacological therapies that may be applicable to the associated brain injury. Overall, more studies are needed to assess the effects of hyperoxia on the immature brain, particularly combined analyses of the lungs and brain in the same experimental setting, to elucidate the potential causes of combined neurodevelopmental impairment in BPD.