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• The ductus arteriosus allows blood to flow from the pulmonary artery to the aorta during fetal life.
• Failure of the normal closure of this vessel results in a PDA .
• With a falling pulmonary vascular resistance after birth, left-to-right shunting of blood and increased pulmonary blood flow occur.
• Excluding premature infants, PDAs = 5%-10% of congenital heart disease.
Closure of the Ductus Arteriosus
Functional closure of the ductus arteriosus occurs within 10 to 15 hours after birth by constriction of the medial smooth muscle in the ductus. Anatomic closure is completed by 2 to 3 weeks of age by permanent changes in the endothelium and subintimal layers of the ductus.
Oxygen, prostaglandin E2 (PGE2) levels, and maturity of the newborn are important factors in closure of the ductus. Acetylcholine and bradykinin also constrict the ductus.
Oxygen and the Ductus.
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.
. A decrease in PGE2 levels after birth results in
1constriction of the ductus.
This decrease results from removal of the placental source of PGE2 production at birth and from the marked increase in pulmonary blood flow, which allows effective removal of circulating PGE2 by the lungs.
Constricting effects of indomethacin or ibuprofen and the dilator effects of PGE2 and PGI2 are greater in the ductal tissues of an immature fetus than of a near-term fetus.
Prolonged patency of the ductus can be maintained by intravenous infusion of a synthetic PGE1, in newborn infants such as those with pulmonary atresia, whose survival depends on patency of the ductus.
Indomethacin or ibuprofen, a cyclooxygenase inhibitor (or “PG synthetase inhibitor”),can be used to close a significant PDA in premature infants .
Maternal ingestion of a large amount of aspirin, an inhibitor of PG synthetase, may harm fetuses, because the aspirin may constrict the ductus during fetal life and may result in persistent pulmonary hypertension in the newborn (PPHN).
It has been suggested that some cases of PPHN (or persistent fetal circulation syndrome) may be caused by a premature constriction of the ductus arteriosus.
Reopening of a Constricted Ductus. Before true anatomic closure occurs, the
functionally closed ductus may be dilated by a reduced arterial Po2 or an increased PGE2 concentration.
The reopening of the constricted ductus may occur in asphyxia and various pulmonary diseases (as hypoxia and acidosis relax ductal tissues).
Ductal closure is delayed at high altitude.
There is a much higher incidence of PDA at high altitudes than at sea level. In some newborn infants (e.g., those with coarctation of the aorta) intravenous infusion of PGE1, can open a partially or completely constricted ductus.
Responses of Pulmonary Artery and Ductus Arteriosus to Various Stimuli.
The PA responds to oxygen and acidosis in the opposite manner from the ductus arteriosus.
Hypoxia and acidosis relax the ductus arteriosus but constrict the pulmonary arterioles.
Oxygen constricts the ductus but relaxes the pulmonary arterioles.
The PAs are also constricted by sympathetic stimulation and α-adrenergic stimulation (e.g., epinephrine,norepinephrine). Vagal stimulation, β-adrenergic stimulation (e.g. isoproterenol), and bradykinin dilate the PAs.