What keeps the ductus arteriosus open during fetal life?

The ductus arteriosus is kept patent in fetal life by circulating prostaglandins (especially prostaglandin E2) and the low oxygen tension of fetal blood.

At birth, the rise in oxygen and the fall in prostaglandin E2 (the placenta, a source, is removed) stimulate ductal constriction and closure. This is the basis for using prostaglandin E to keep it open, or NSAIDs to close it.

Clinical relevance. Prostaglandins and low oxygen maintain ductal patency - the pharmacological basis for opening/closing the duct in neonates.

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Maintaining ductal patency in the fetus

Prostaglandins and low oxygen keep the ductus arteriosus open before birth.

What keeps it open

• Prostaglandin E2 (and prostaglandin I2) - actively relax the ductal smooth muscle.
• The low oxygen tension of fetal blood also favours patency.
• The placenta is a source of prostaglandins and clears little of them, keeping circulating levels high.

What closes it at birth

• The rise in arterial oxygen tension (after the first breath) constricts the ductus.
• The fall in prostaglandin E2 (the placenta is removed, and pulmonary clearance increases) removes the dilating stimulus.

Clinical relevance

• Prostaglandin E (alprostadil) infusion keeps the ductus open in duct-dependent congenital heart disease.
• NSAIDs (ibuprofen/indometacin) close a patent ductus arteriosus by inhibiting prostaglandin synthesis.