Abstract
The fetus is exposed to chronic low oxygen environment, which is a desirable physiological condition for fetal pulmonary development and hemodynamics. On the other hand, if the newborn is exposed to low oxygen levels, the blood vessels of the lung thicken and narrow due to overgrowth of the smooth muscle cells in the vessel walls, the baby remains blue, resulting in the condition known as persistent pulmonary hypertension of the newborn (PPHN). In the United States, PPHN occurs in 0.43-6.8 newborns per 1000 live births and is most common in term and near-term newborns. Despite the significant advances in management of newborn respiratory diseases, PPHN is still associated with a high morbidity and mortality, accounting for about 10-20% of neonatal mortality. The current mainstay of therapy for PPHN is mechanical ventilation, fluid therapy and use of anti-inflammatory agents for cardiovascular support. Correction of hemodynamic acid/base balance and oxygen supplementation are also commendable therapeutic interventions. New ideas in PPHN therapy should include incorporation of in vivo, ex vivo and in vitro studies on intracellular signaling pathways of pulmonary vascular development in the state of PPHN. These new ideas will entail studies of the cross talk between vasodilators and vasoconstrictors in perinatal pulmonary hemodynamics.