A neonate born at 34 weeks gestation has echocardiographic evidence of duct-dependent congenital heart disease requiring maintenance of ductal patency until surgery. Which endogenous mediator physiologically sustains ductal patency, and which drug class would be expected to close the duct prematurely?
- A LTB4; calcium channel blockers
- B PGI2; corticosteroids
- C TXA2; selective serotonin reuptake inhibitors
- D PGE2; NSAIDs such as indomethacin ✓
Explanation
Prostaglandin E2, produced locally in the ductus arteriosus, keeps the vessel relaxed and patent in fetal life. Prostaglandin levels fall after birth, allowing constriction. NSAIDs inhibit prostaglandin synthesis via COX and are deliberately given (for example indomethacin or ibuprofen) to close a hemodynamically significant patent ductus arteriosus, whereas intravenous PGE1 (alprostadil) is infused therapeutically to maintain patency.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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