In the fetal circulation, the ductus arteriosus directs blood from the pulmonary artery to the aorta. At birth, the ductus arteriosus closes functionally within hours. The primary physiological trigger for this closure is:

• A Increased prostaglandin E2 release from the lungs upon ventilation
• B Bradykinin release from the lungs acting on ductal smooth muscle receptors
• C Rise in arterial PO2 following the first breath, causing smooth muscle contraction in the ductal wall ✓
• D Fall in pulmonary vascular resistance reducing right-to-left ductal flow, allowing passive recoil

Explanation

The functional closure of the ductus arteriosus is primarily triggered by the rise in PaO2 that occurs immediately after birth when the newborn takes the first breath. Increased oxygen tension directly contracts the oxygen-sensitive smooth muscle in the ductal wall through inhibition of K+ channels (similar to HPV mechanism in reverse), causing depolarization and vasoconstriction. Prostaglandin E2 (PGE2) actually keeps the ductus patent in fetal life; its clearance by the now-ventilated lungs also contributes to closure, but the oxygen-mediated mechanism is primary and rapid. Indomethacin (COX inhibitor) is used therapeutically to close a PDA by reducing PGE2.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.