title: Evaluation of progesterone deficiency as a cause of fetal death in mares with experimentally induced endotoxemia.
abstract: The role of decreased luteal activity in embryonic loss after induced endotoxemia was studied in mares 21 to 35 days pregnant. Fourteen pregnant mares were treated daily with 44 mg of altrenogest to compensate for the loss of endogenous progesterone secretion caused by prostaglandin F2 alpha (PGF2 alpha) synthesis and release following intravenous administration of Salmonella typhimurium endotoxin. Altrenogest was administered daily from the day of endotoxin injection until day 40 of gestation (group 1; n = 7), until day 70 (group 2; n = 5), or until day 50 (group 3; n = 2). In all mares, secretion of PGF2 alpha, as determined by the plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations, followed a biphasic pattern, with an initial peak at 30 minutes followed by a second, larger peak at 105 minutes after endotoxin injection. Plasma progesterone concentrations decreased in all mares to values less than 1 ng/ml within 24 hours after endotoxin injection. In group 1, progesterone concentrations for all mares were less than 1 ng/ml until the final day of altrenogest treatment. In 6 of 7 mares in group 1, the fetuses died within 4 days after the end of treatment, with progesterone concentrations less than 1 ng/ml at that time. In the mare that remained pregnant after the end of treatment, plasma progesterone concentration was 1.6 ng/ml on day 41 and increased to 4.4 ng/ml on day 44. In group 2, all mares remained pregnant, even though plasma progesterone concentrations were less than 1 ng/ml in 4 of 5 mares from the day after endotoxin injection until after the end of altrenogest treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Reproduction, School of Veterinary Medicine, University of California, Davis 95616.
authors.forename: P F
authors.initials: PF
authors.lastname: Daels
authors.forename: G H
authors.initials: GH
authors.lastname: Stabenfeldt
authors.forename: J P
authors.initials: JP
authors.lastname: Hughes
authors.forename: K
authors.initials: K
authors.lastname: Odensvik
authors.forename: H
authors.initials: H
authors.lastname: Kindahl
mesh_terms: D000818:Animals; D015237:Dinoprost / Q000097:blood / Q000378:metabolism*; D004731:Endotoxins / Q000097:blood / Q000633:toxicity*; D005069:Evaluation Studies as Topic; D005260:Female; D005313:Fetal Death / Q000209:etiology / Q000662:veterinary; D006734:Horse Diseases / Q000097:blood / Q000139:chemically induced*; D006736:Horses; D011247:Pregnancy; D011255:Pregnancy Maintenance / Q000187:drug effects; D011374:Progesterone / Q000037:antagonists & inhibitors / Q000097:blood / Q000172:deficiency*; D012486:Salmonella typhimurium; D012772:Shock, Septic / Q000139:chemically induced / Q000150:complications / Q000662:veterinary*; D014204:Trenbolone Acetate / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D004731:Endotoxins; C023445:altrenogest; D011374:Progesterone; D015237:Dinoprost; D014204:Trenbolone Acetate