Abstract
Ewes were lutectomized and treatments were started 72 h later. Pregnant ewes were treated with vehicle; prostaglandin F 2α (PGF 2α); cortisol (C); trilostane (TR), a 3β-hydroxy-steroid dehydrogenase inhibitor; PGF 2α + C; TR + PGF 2α; TR + C, or TR + PGF 2 + C. TR, TR + PGF 2α, TR + C, and TR + PGF 2α + C aborted ( P ≤ 0.05) all ewes receiving TR. One ewe treated with PGF 2α aborted ( P ≥ 0.05). The average time to abortion of TR-treated ewes was 50.8 h ( P ≤ 0.05) after initiation of treatments. All aborted ewes had retained placentas ( P ≤ 0.05) except one ewe in the TR + PGF 2α, treatment group. TR was given every 12 h starting at 72 h postlutectomy until 96 h postlutectomy. TR reduced ( P ≤ 0.05) progesterone. Estradiol-17β was increased ( P ≤ 0.05) 2 h after the first two TR treatments and declined 2 h later and was followed by a sustained increase ( P ≤ 0.05) in estradiol-17β, which was coincident with the onset of abortions. Estradiol-17β was increased ( P ≤ 0.05) by PGF 2α but did not decrease ( P ≥ 0.05) placental secretion of progesterone. It is concluded that TR but not PGF 2α is an abortifacient in 90-day-pregnant lutectomized ewes and that abortion occurs only when there is a decrease in circulating progesterone and an increase in circulating estradiol-17β.
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