Neonatal Hyperoxia and Pulmonary Hypertension

Miranda Sun and Qiwei Yang*

Neonatal Hyperoxia and Pulmonary Hypertension.

Oxygen therapy and mechanical ventilation with hyperoxia are necessary to treat patients with respiratory distress and failure. However, premature infants requiring oxygen supplementation and ventilation often develop Bronchopulmonary Dysplasia (BPD) as a chronic lung disease, and Pulmonary Hypertension (PH) occurs in 25% to 35% of premature infants with significant BPD. Recent reports indicate that the morbidity and mortality from pulmonary hypertension due to BPD is high, with up to 48% mortality 2 years after the diagnosis of PH.

The effects of adverse environmental factors on a newborn’s lungs lead to the failure of the pulmonary circulation to fully adapt to postnatal life. This, in turn, contributes to the pathogenesis of pulmonary vascular dysfunction later in life. There is increasing evidence in humans and experimental animal models that exposure to neonatal hyperoxia results in factors that may be linked to the development of pulmonary vascular disease and hypertension. The focus of this review is to elaborate on hyperoxiaactivated key sensing molecules and signaling pathways, summarized in Figure 1 and Table 1, in neonatal hyperoxia-induced PH.

Hyperoxic ventilation in the management of Persistent Pulmonary Hypertension of the Newborn (PPHN) results in the formation of reactive oxygen species, such as superoxide anions, which can inactivate Nitric Oxide (NO) and cause vasoconstriction and oxidation.

PDEs hydrolyze the cyclic nucleotide second messengers of important pulmonary vasodilator agents, including prostacyclin and NO.8 In vitro data have shown that hyperoxia increases PDE5 expression and activity in ovine fetal Pulmonary Artery Smooth Muscle Cells (PASMCs).


Pediatr Neonatal Nurs Open J. 2014; 1(1): 1-5. doi: 10.17140/PNNOJ-1-101