Ductus arteriosus

Ductus arteriosus
Plan of the fetal circulation. ("Ductus arteriosus" visible at upper right.)
Heart cross-section with PDA
Details
Latin	Ductus arteriosus
Precursor	aortic arch 6
Source	pulmonary artery
Branches	descending aorta
Vein	ductus venosus
Identifiers
MeSH	A07.541.278.395
Dorlands /Elsevier	d_29/12314749
TA
TH	{{#property:P1694}}
TE	{{#property:P1693}}
FMA	{{#property:P1402}}
Anatomical terminology [[[d:|edit on Wikidata]]]

In the developing fetus, the ductus arteriosus, also called the ductus Botalli, is a blood vessel connecting the pulmonary artery to the proximal descending aorta. It allows most of the blood from the right ventricle to bypass the fetus's fluid-filled non-functioning lungs. Upon closure at birth, it becomes the ligamentum arteriosum. There are two other fetal shunts, the ductus venosus and the foramen ovale.

Structure

The ductus arteriosus attaches to the final part of the arch of aorta (the isthmus of aorta) and the first part of the [pulmonary artery]

Clinical significance

Patent ductus arteriosus

Main article: Patent ductus arteriosus

Failure of the DA to close after birth results in a condition called patent ductus arteriosus and the generation of a left-to-right shunt. If left uncorrected, patency leads to pulmonary hypertension and possibly congestive heart failure and cardiac arrhythmias.

The E series of prostaglandins are responsible for maintaining the patency of the DA (by dilation of vascular smooth muscle) throughout the fetal period. 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. PGE₁ and PGE₂ keep the DA open via involvement of specific PGE-sensitive receptors (such as EP2 or EP4). EP4 is the major receptor associated with PGE₂-induced dilation of the DA and can be found across the DA in smooth muscle cells. Immediately after birth, the levels of both PGE₂ and the EP4 receptors reduce significantly, allowing for closure of the DA and establishment of normal postnatal circulation..

In some types of congenital heart defect (e.g., transposition of the great arteries), prostaglandins may be administered to maintain DA patency, allowing for the continual circulation and oxygenation of blood, until surgery can be performed.

DA closure may be induced by administration of nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit prostaglandin production. The most common NSAID that is used to force DA closure is Indomethacin, which can be administered after birth. 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. 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.

A patent ductus arteriosus affects approximately 4% of infants with Down syndrome (DS). A failure to thrive is a very common sign of this condition.

See also

Ductus venosus

This article uses anatomical terminology; for an overview, see Anatomical terminology.

External links

• Circulatory changes at birth at berkeley.edu