Journal of Reproduction and Development
Online ISSN : 1348-4400
Print ISSN : 0916-8818
ISSN-L : 0916-8818
Original Article
Incidence of Abnormal Corpus Luteum in Superovulated Ewes
Aki OKADASyuhei KAMADAChun-Woo JEONAkio MIYAMOTOYutaka FUKUI
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JOURNAL FREE ACCESS

2000 Volume 46 Issue 6 Pages 397-402

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Abstract
In the present study, in order to investigate the incidence time of abnormal corpus luteum (CL) in superovulated ewes, CL formation was observed and plasma progesterone (P4) and estradiol-17β(E2) profiles were investigated during the non-breeding and breeding seasons in three breeds of ewes. The ewes were treated with a fluorogesterone acetate (FGA) sponge for 12 days, and a single injection of 20 mg pFSH on Day - 2 and 500 IU eCG on Day - 1 (FGA sponge removal: Day 0), for estrous synchronization and superovulation. All ewes were given an injection of 100 μg gonadotropin releasing hormone analogue (GnRH analogue) at estrous detection and inseminated with frozen-thawed semen by laparoscope on a fixed-time basis (32-36 h after FGA sponge removal). On Day 6.5, the ewes were laparotomized for ovarian response and embryo recovery. Blood was taken from all ewes on Days 0 to 6.5, and the plasma P4 and E2 concentrations were measured by emzyme immunoassay (EIA). According to the ovarian responses on Day 6.5, the ewes were divided into Group N (only normal CL; n=21), Group A (only abnormal CL; n=7) and Group M (both normal and abnormal CL; n=3). The mean P4 profile in Group N continued to rise during the period of blood sampling, and was significantly higher than in Group A which remained under 1 ng/ml and decreased after Days 4 to 4.5. The means E2 levels tended to be higher in Group A than in Group N. In the autumn study, the ewes with abnormal CL on Day 6.5 had already lacked in color on Day 4.5, and the number of large follicles was significantly lower in the ewes with abnormal CL than in those with only normal CL. These results indicate that the phenomenon of abnormal CL formation at 3-3.5 days after estrus is not due to premature luteal regression of functionally complete CL, but to luteal hypoplasia of incomplete CL with a short lifespan, but the cause of abnormal CL was not determined in the study.
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© 2000 Society for Reproduction and Development

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https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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