What causes patent ductus arteriosus (PDA) in preterm infants?

Updated: Nov 20, 2018
  • Author: Luke K Kim, MD; Chief Editor: Stuart Berger, MD  more...
  • Print

Failure of ductus arteriosus contraction in preterm neonates has been suggested to be due to poor prostaglandin metabolism because of immature lungs. Furthermore, high reactivity to prostaglandin and reduced calcium sensitivity to oxygen in vascular smooth muscle cells contribute to contraction of the ductus. The absence of ductus arteriosus contraction in full-term neonates might be due to failed prostaglandin metabolism most likely caused by hypoxemia, asphyxia, or increased pulmonary blood flow, renal failure, and respiratory disorders.

Cyclooxygenase (COX)-2 (an isoform of COX-producing prostaglandins) induction and expression might also prevent ductal closure. The activation of G protein-coupled receptors EP4 by PGE2, the primary prostaglandin regulating ductal tone leads to ductal smooth muscle relaxation.

During late gestation, the decrease in prostaglandin levels results in constriction of the ductus arteriosus. Thus, the intimal cushions come into contact and occlude the ductus lumen.

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!