Phenotypical Changes of the Pulmonary Artery Endothelial Cells in Fetal Sheep Model of Persistent Pulmonary Hypertension of the Newborn

Persistent pulmonary hypertension of the newborn is a disorder with failure to decrease pulmonary vascular resistance after birth. Persistent pulmonary hypertension of the newborn happens in one out of 500 live births with a mortality rate 10-50%. Right after birth the pulmonary vascular resistance decreases drastically within a few minutes when oxygen enters into the fluid-filled alveoli. Failure to achieve this transition impairs adequate blood flow into the lungs to be oxygenated. There are several mechanisms that can impede this transition such as decreased blood vessel count in the lungs or inadequate production of vasorelaxant by the endothelial cells. The most important vasorelaxants to the pulmonary vasculature are nitric oxide [1] and prostacyclin [2]. Endothelial cells also produce vasoconstricting substance such as endothelin-1. It is believed that the surge of ATP formation by the pulmonary vasculature right after birth is the agonist that prompts the release of nitric oxide and prostacyclin from the pulmonary vasculature [1]. There is evidence to suggest that the productions of nitric oxide and prostacyclin are impaired in persistent pulmonary hypertension of the newborn whereas formation of endothelin-1 is increased. Several animal models have been used to study persistent pulmonary hypertension of the newborn and readers