Abstract
The ductus arteriosus is kept patent in the fetus by a process involving prostaglandin (PG) E2, both local and blood-borne, as the main effector [1]. The PGE2-based relaxing mechanism develops early in gestation and, in fact, with a premature birth its intramural component may prevail over the oxygen constriction [1]. This knowledge has, on one hand, introduced indomethacin in the management of prematurely born infants with persistent ductus and, on the other hand, has highlighted potential detrimental effects on the unborn child of nonsteroidal anti-inflammatory drugs taken by the mother. The realization now that PGE2 may originate from two cyclooxygenase (COX) isoforms, COX1 and COX2, has added complexity but, at the same time, has broadened the scope of any therapeutic intervention.
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Coceani, F., Ackerley, C., Seidlitz, E., Kelsey, L. (2001). Cyclooxygenase in the Lamb Ductus Arteriosus: Developmental Changes and Upregulation. In: Samuelsson, B., Paoletti, R., Folco, G.C., Granström, E., Nicosia, S. (eds) Advances in Prostaglandin and Leukotriene Research. Medical Science Symposia Series, vol 16. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9721-0_26
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DOI: https://doi.org/10.1007/978-94-015-9721-0_26
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