Abstract
It is well accepted that patency of the ductus arteriosus in the fetus is an active process being sustained primarily by prostaglandin E2 (PGE2) but conceivably involving other agents, nitric oxide (NO) in particular [1]. Previous investigations, using lamb and pig, have shown that cyclooxygenases (COXs) develop unevenly within the ductus wall, with COX1 preceding COX2 through the last third of gestation [[2]–[4]], Therefore, both enzymes have been implicated in PGE2 synthesis at term, while COX1 has been assigned a greater role in the premature [4]. In contrast with these findings, however, it has recently been reported that the term mouse ductus is normally missing COX1 and may, accordingly, fail to constrict to indomethacin (given to the mother) once its COX2 has also been deleted [5]. A separate investigation, on the other hand, could not demonstrate any significant evidence of either enzyme in the same vessel [6].
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Coceani, F., Baragatti, B., Brizzi, F., Barogi, S., Ackerley, C. (2003). Cyclooxygenase (COX) Function in the Ductus Arteriosus: Another Look. In: Yazici, Z., Folco, G.C., Drazen, J.M., Nigam, S., Shimizu, T. (eds) Advances in Prostaglandin, Leukotriene, and other Bioactive Lipid Research. Advances in Experimental Medicine and Biology, vol 525. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9194-2_41
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DOI: https://doi.org/10.1007/978-1-4419-9194-2_41
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