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West Virginia University1, Morgantown 26506-6108
Abstract
To examine effects of norgestomet pretreatment on development of follicles and their response to administration of gonadotropin releasing hormone (GnRH), 45 pluriparous suckled beef cows were assigned at random to receive a 6-mg implant of norgestomet for 9 d (inserted 24 d postpartum) or serve as untreated controls. Ovaries were obtained 48 h after removal of implants or 10 to 11 or 20 to 22 h after im administration of 150 µg GnRH at 48 h after removal of the implant. The largest follicle (F1 and all follicles within 3 mm in diameter of the F1 were dissected from the ovaries. Theca, granulosa and follicular fluid were separated and assayed for steroids and prostaglandins. Diameters and weights of F1 and weights of follicular components remained unchanged in control cows, but increased by 10 h and declined by 20 h in norgestomet-pretreated cows (treatment x time, quadratic, P<.05). Ovarian volume and numbers of follicles at the surface of the ovary did not differ with treatment, but the diameter of the second-largest follicle (F2) was smaller (P<.05) in norgestomet-pretreated cows than in controls (6.0 ± .9 vs 8.2 ± .7 mm). The F1 were embedded in the ovary in fewer norgestomet-pretreated than control cows (2/22 vs 8/23; P<.05). Changes in steroids in F1 paralleled those in size (treatment x time, quadratic, P<.05). Overall, F1 from norgestomet-pretreated cows had higher (P<.05) contents of estradiol. Contents of prostaglandins in F1 follicles did not differ with treatment, but increased (P<.05) following treatment with GnRH. The F2 had lower contents of estradiol than F1. It is suggested that norgestomet effected the maturation of a single follicle which produced more estradiol.
1 Div. of Anim. and Vet. Sci. Published with the approval of the Director of the West Virginia Agr. and For. Exp. Sta. as scientific paper no. 2039. Supported by Hatch Project 224 (NE-72) and USDA Grant 83-CRSR-2-2190. The authors are indebted to Dr. John Pike, The Upjohn Co., for assay standards for prostaglandins; to Dr. Lawrence Levine, Brandeis Univ., for antiserum to PGF2
; Dr. Norman Mason, Eli Lilly and Co., for antiserum to PGE2; to Dr. Gordon Niswender, Colorado State Univ., for antiserum to LH; to Natl. Inst. of Arthritis, Metabolism and Digestive Diseases, for antiserum to FSH and standards; to Dr. R. L. Butcher, West Virginia Univ., for antiserum to progesterone; and to Dr. E. Henderson, Ceva Laboratories, for norgestomet implants and GnRH. We thank Dr. R. A. Dailey, West Virginia Univ., for valuable discussions of follicular physiology, Dr. Douglas Vincent and Ms. Phyllis Jenkins for the assays of prostaglandins, and Ms. Mary Ann Barnes for her patience in preparation of the manuscript.
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