Abstract
Eicosanoid production by intrauterine tissues from control and neonatal-steptozotocin induced diabetic rats during late pregnancy was evaluated. In diabetic placenta the release of 6-keto-PGF 1α was found diminished when compared to controls. In addition, LTB 4 generation was increased in diabetic placenta. No alterations in the production of TXA 2, PGE 2, PGE 1 and PGF 2α was found when diabetic and control placenta were compared. In amnion tissue a decreased generation of 6-keto-PGF 1α was observed in the diabetic group, but no alteration in any other eicosanoid evaluated was found. Oxytocin (5 mU/ml, in vitro), which increases prostaglandin synthesis in rabbit and human amnion tissues, did not modify eicosanoid generation in control rat amnion. In contrast, in diabetic amnion the presence of oxytocin further decreased the release of 6-keto-PGF 1α and diminished PGE 1 generation. The present results suggest that this mildy diabetic state induces alterations in eicosanoid production in intrauterine tissues, abnormalities probably enhanced during parturition, when endogenous concentrations of oxytocin are elevated.
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