It has been speculated that hypoxia might cause vasodilation of the ductus arteriosus by enhancing the relaxing action of endogenous prostaglandins. Using isolated rings of lamb ductus arteriosus, we measured immunoreactive PGE2 released into the bath solution. We found that after a period of stabilization following suspension of the rings in low PO2, only a negligible amount of PGE2 was released by the rings (1.15 ± 0.52 pg PGE2/mg wet weight per 45 min, n14, ±SEM). When rings were exposed to a high PO2, significant amounts of PGE2 were released (32.3 ± 12.6 pg PGE2/mg wet weight per 45 min). These observations were supported by our findings that indomethacin had a negligible contractile effect (0.11 ± 0.09 g/mm2, n=11) on rings equilibrated in a low PO2, but caused a significant contraction (0.55 ± 0.12 g/mm2, n=11) in rings incubated in a high PO2. These findings do not support the hypothesis that low PO2 increases PGE2 production by the lamb ductus arteriosus. They are consistent with the hypothesis that endogenous PGE2 inhibits the ability of the vessel to contract in response to oxygen. In addition (if these in vitro results can be extrapolated to the in vivo situation), the demonstration that the ductus arteriosus needs an oxygen tension greater than that present in utero to produce effective amounts of PGE2, strengthens the hypothesis that circulating levels of PGE2 may be important in the prenatal maintenance of ductal patency.
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