Prostanoid concentrations in maternal/fetal plasma and amniotic fluid and intrauterine tissue prostanoid output in relation to myometrial contractility during the onset of adrenocorticotropin-induced preterm labor in sheep.
Prostanoid [prostaglandin (PG)] concentrations were measured in ovine maternal and fetal plasma and amniotic fluid during the onset of preterm labor induced by the administration of a pulsatile infusion of ACTH-(1-24) (P-ACTH; 66.7 ng/min for 15 min every 2 h) to the fetus and in saline-infused controls. P-ACTH administration stimulated a change in intra-uterine pressure from type A-activity, characterized by sustained increases of low amplitude, to type B labor-like activity of short duration, high amplitude (greater than or equal to 10 mm Hg) increases which occurred between 12 and 8 h before the onset of labor. PGF2 alpha and/or PGFM (13,14-dihydro-15-keto PGF2 alpha) concentrations increased consistently in all fluids 16 h or earlier before labor. All PGs increased in fetal carotid arterial plasma (PGE2 greater than PGF2 alpha) and amniotic fluid, and the relative increases in each PG were similar. However, PGF2 alpha and PGFM selectively increased in maternal vena caval and aortic plasma, whereas smaller or negligible increases in the prostacyclin hydrolysis metabolite 6-keto PGF1 alpha (6KF) and PGE2 were noted. The output of PGs E2 and F2 alpha (picograms per 10(5) cells/8 h) increased 1.6- and 1.7-fold, respectively, by cells dispersed from the chorioallantois of P-ACTH-treated animals compared to that in control animals infused with saline for 100 h. From fetal cotyledons, these increases were 2.4-fold (P less than 0.05) and 3.6-fold, respectively. No significant changes occurred in 6-keto PGF1 alpha output from any tissue or PGE2 or PGF2 alpha output from amnion or maternal cotyledons. We conclude 1) that PGs increase in all fluids before the increase in uterine mechanical activity during induced preterm labor, implying that PGs mediate this event and are not a result thereof; 2) that syntheses of PGs E2 and F2 alpha increase similarly in intrauterine tissues with the onset of labor; and 3) that a selective increase in PGF2 alpha, a myometrial stimulatory PG, occurs exclusively in maternal plasma, suggesting that endoperoxide conversion to PGF2 alpha is specifically enhanced during parturition or suggesting the existence of an intrauterine tissue source of 9-keto PG reductase.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000650:Amnion / Q000378:metabolism; D000653:Amniotic Fluid / Q000378:metabolism*; D000818:Animals; D002823:Chorion / Q000378:metabolism; D003366:Cosyntropin; D015237:Dinoprost / Q000031:analogs & derivatives; D015232:Dinoprostone; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D007752:Obstetric Labor, Premature / Q000139:chemically induced / Q000378:metabolism*; D011247:Pregnancy; D011453:Prostaglandins / Q000097:blood / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D012756:Sheep; D014590:Uterine Contraction; D014599:Uterus / Q000378:metabolism*
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D003366:Cosyntropin; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D015232:Dinoprostone