Ductus arteriosus

right ventricle to bypass the fetus's fluid-filled non-functioning lungs. Upon closure at birth, it becomes the ligamentum arteriosum.^{[clarification needed}

isthmus of aorta) and the first part of the pulmonary artery.^[2]

cardiac arrhythmias

prostaglandins are responsible for maintaining the openness of the ductus arteriosus (by dilation of vascular smooth muscle) throughout the fetal period.^[3] Prostaglandin E2 (PGE₂), produced by both the placenta and the DA itself, is the most potent of the E prostaglandins, but prostaglandin E1 (PGE₁) also has a role in keeping the DA open.^[4] PGE₁ and PGE₂ keep the ductus arteriosus open via involvement of specific PGE-sensitive receptors (such as EP4 and EP2).^[5] EP4 is the major receptor associated with PGE₂-induced dilation of the DA and can be found across the DA in smooth muscle cells.^[6]

Indomethacin, which is usually administered in the first week after birth.^[4] However, in the presence of a congenital defect with impaired lung perfusion (e.g. Pulmonary stenosis and left-to-right shunt through the ductus), it may be advisable to improve oxygenation by maintaining the ductus open with prostaglandin treatment. However, such treatments are ineffective in an abnormal ductus. Persistence of the ductus may be associated with other abnormalities, and is much more common in females. By inhibiting PGE₂ formation, EP4 receptor activation will decrease and normal circulation can begin. NSAIDs taken late in pregnancy can cross the placenta and lead to premature closure of the DA in the fetus.^[7] In this case, exogenous PDE₂ can be administered to reverse the effects of the NSAIDs and maintain the patency of the DA for the remainder of the pregnancy.^[4]

transposition of the great arteries), prostaglandins may be administered to maintain the DA open, allowing for the continual circulation and oxygenation of blood, until surgery can be performed.^[9]