A postnatal increase in oxygen saturation of the systemic circulation (from Po2 of 25 mm Hg in utero to 50 mm Hg after lung expansion) is the strongest stimulus for constriction of the ductal smooth muscle, which leads to closure of the ductus.
The responsiveness of the ductal smooth muscle to oxygen is related to the gestational age of the newborn; the ductal tissue of a premature infant responds less
intensely to oxygen than that of a fullterm infant.
This decreased responsiveness of the immature ductus to oxygen is due to its decreased sensitivity to oxygen-induced
contraction; it is not the result of a lack of smooth muscle development because the immature ductus constricts well in response to acetylcholine.
It may also be due to persistently high levels of PGE2 in preterm infantsProstaglandin E and the Ductus.
A few clinical situations are worth mentioning to show the importance of the PG series in maintaining the patency of the ductus arteriosus in fetuses.