Ductus arteriosus

Ductus arteriosus

Plan of the fetal circulation. ("Ductus arteriosus" visible at upper right.)

Heart cross-section with PDA
Details
Precursor aortic arch 6
Source pulmonary artery
Branches descending aorta
Vein ductus venosus
Identifiers
Latin Ductus arteriosus
MeSH A07.541.278.395
Dorlands
/Elsevier		 d_29/12314749
TE E5.11.2.1.2.0.17
FMA 79871

Anatomical terminology

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][1]

Clinical significance

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.[2] 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.[3] PGE1 and PGE2 keep the DA open via involvement of specific PGE-sensitive receptors (such as EP2 or EP4).[4] EP4 is the major receptor associated with PGE2-induced dilation of the DA and can be found across the DA in smooth muscle cells.[5] 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.[6]

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.[7]

DA closure may be induced by administration of nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit prostaglandin production.[8] The most common NSAID that is used to force DA closure is Indomethacin, which can be administered after birth.[9] 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.[10] 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.[11]

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.[12]

See also

Ductus venosus

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

References

  1. ↑ Srichai, editors, David P. Naidich ... [et al.] ; contributing author, Monvadi B. (2007). Computed tomography and magnetic resonance of the thorax (4th ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. p. 100. ISBN 9780781757652.
  2. ↑ "Prostaglandins and the ductus arteriosus". The Lancet.
  3. ↑ Olley, P.M.; Conceani F. (1981). "Prostaglandins and the Ductus Arteriosus". Annual Review of Medicine 32 (1): 375–385. doi:10.1146/annurev.me.32.020181.002111.
  4. ↑ Bouayad, D.R.; Kajini W., Waleh N., Fouron J. Andelfinger A., Vazquez A., Gobeil F., Clyman R., Chemtob S. (1 May 2001). "Characterization of PGE2 Receptors in fetal and newborn lamb ductus arteriosus". American Journal of Physiology. Heart and Circulatory Physiology 280 (5): 2342–2349. Cite uses deprecated parameter |coauthors= (help)
  5. ↑ Gruzdeva, A; Nguyena, M.; Kovarovob, M.; Koller, B (March 2012). "PGE2 through the EP4 receptor controls smooth muscle gene expression patterns in the ductus arteriosus critical for remodeling at birth.". Prostaglandins and other Lipid Mediators 94 (3): 109–119. doi:10.1016/j.prostaglandins.2012.02.001.
  6. ↑ Gruzdeva, A.; Nguyena, M.; Kovarovob, M.; Koller, B. (March 2012). "PGE2 through the EP4 receptor controls smooth muscle gene expression patterns in the ductus arteriosus critical for remodeling at birth.". Prostaglandins and other Lipid Mediators 94 (3): 109–119. doi:10.1016/j.prostaglandins.2012.02.001.
  7. ↑ "Congenital heart defects: Prostaglandins and prostaglandin inhibitors.". Healthwise. My Health Alberta.
  8. ↑ Olley, P.M.; COnceani F. (1981). "Prostaglandins and the ductus arteriosus". Annual Review of Medicine 32 (1): 375–385. doi:10.1146/annurev.me.32.020181.002111.
  9. ↑ Olley, P.M; Conceani F. (1981). "Prostaglandins and the ductus arteriosus". Review of Medicine 32 (1): 375–385. doi:10.1146/annurev.me.32.020181.002111.
  10. ↑ Anonucci, R; Zaffanello, M.; Puxeddu, E.; Porcella, A.; Cuzzolin, L.; Pilloni, M.; Fanos, V. (2012). "Use of non-steroidal anti-inflammatory drugs in pregnancy:impact on the fetus and newborn". Current Drug Metabolism 13 (4): 474–490. doi:10.2174/138920012800166607.
  11. ↑ Olley, P.M; Conceani F. (1981). "Prostaglandins and the ductus arteriosus". Annual Review of Medicine 32 (1): 375–385. doi:10.1146/annurev.me.32.020181.002111.
  12. ↑ Pritchard & Korf. "Medical Genetics at a Glance". Blackwell Publishing. 2010. p63.

External links

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