Prostaglandin H synthase activity in the sheep placenta during cortisol-induced labor at 128–131 days of gestation and during spontaneous delivery at term

Jeffrey Wimsatt, Peter W. Nathanielsz
In: Prostaglandins, Leukotrienes and Essential Fatty Acids · 1995 · vol. 53(1) , pp. 53–58 · doi:10.1016/0952-3278(95)90083-7 · PMID:7675823 · W2088253284
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This study found that cortisol did not induce prostaglandin H synthase activity in sheep placenta at 128–131 days of gestation, while spontaneous labor significantly diminished enzyme activity due to decreased PGE2 production.

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Abstract

This study investigated whether the prostaglandin H synthase (PGHS) enzyme activity of sheep fetal placental cotyledon can be induced by cortisol at 128-131 days of gestation (dga) as compared to gestational age matched controls, before PGHS's normal gestational increase would occur (experiment 1). This study also investigated whether active PGHS is diminished following prostanoid synthesis in the labor process (experiment 2). A PGHS activity assay was employed in which PGE2 product was measured under initial velocity conditions. Labor was induced before term by continuous infusion of 10 mg of cortisol succinate per day (day 1) followed by 15 mg per day (days 2-4, or until delivery) of cortisol succinate administered through the fetal saphenous vein. Cotyledonary tissue was collected from sheep at term (142-145 dga), as judged by the absence of labor-type myometrial electromyogram (EMG) activity, and during cortisol induction at 128-131 dga. Tissue was also collected from term laboring animals immediately after fetal delivery while the fetus was still attached to the umbilicus and before placental delivery. At 128-131 dga, cortisol had no significant effect on PGHS activity as compared to gestational age matched saline-infused controls; thus, it is unlikely that cortisol directly induces PGHS. In experiment 2, normal progression of active spontaneous labor led to a significant diminution of PGHS activity (p < 0.05) that may be partially explained, based on thin-layer chromatography (TLC) results, as a significant decrease in PGE2 (p < 0.05) production coincident with a lesser compensatory increase in PGD2 (p = 0.06) output.

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