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RECORD NUMBER: 27 OF 32

Main Title Use of Bromoergocryptine in the Validation of Protocols for the Assessment of Mechanisms of Early Pregnancy Loss in the Rat.
Author Cummings, A. M. ; Perreault, S. D. ; Harris, S. T. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;NSI Technology Services Corp., Research Triangle Park, NC.
Publisher c1991
Year Published 1991
Report Number EPA/600/J-91/313;
Stock Number PB92-124692
Additional Subjects Animal pregnancy ; Missed abortion ; Bromocriptine ; Corpus luteum ; Pituitary gland ; Embryo ; Rats ; Ovariectomy ; Progesterone ; Risk assessment ; Organ weight ; Reprints ; Early Pregnancy Protocol
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Status
NTIS  PB92-124692 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 14p
Abstract
Validated protocols for evaluating maternally mediated mechanisms of early pregnancy failure in rodents are needed for use in the risk assessment process. To supplement previous efforts in the validation of a panel of protocols assembled for the purpose, bromoergocryptine (BEC) was used as a model compound because it is known to inhibit pituitary prolactin secretion. BEC was tested using the early pregnancy protocol (EPP), the decidual cell response technique (DCR), the pre- vs postimplantation protocol (PPP), and embryo transport rate analysis (ETRA). These protocols evaluate the effects of chemicals on multiple endpoints following exposure during (1) the first 8 days of pregnancy, (2) early pseudopregnancy accompanied by decidual induction, (3) the pre- and postimplantation intervals of early pregnancy, or (4) the period of embryo transport. In the EPP, dosing with BEC during Days 1-8 of pregnancy reduced the number of implantation sites found on Day 9 as well as serum progesterone. The DCR technique revealed a dose-dependent inhibition of decidual growth concomitant with decreased serum progesterone as a result of BEC treatment. A modified DCR technique using hormone-supplemented ovariectomized rats demonstrated that BEC did not impair decidual growth in the presence of adequate progestogenic support. (Copyright (c) 1991 by the Society of Toxicology.)