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Oklahoma Agricultural Experiment Station, Stillwater 74074 and Department of Agriculture, EL Reno 73036
Abstract
Thirty-one 3-year-old Angus cows and 23 2-year-old Angus heifers were randomly allotted to two treatment groups to examine the influence of PMSG on endocrine and reproductive responses. Sixteen cows and 11 heifers received a single subcutaneous injection of 2,000 IU PMSG on day 17 of the estrous cycle (Trt 17); 15 cows and 12 heifers received 1,500 IU PMSG on day 5 and 2,000 IU on day 17 (Trt 5, 17). Plasma progesterone, estradiol and LH concentrations were quantified in jugular blood collected at regular intervals during the treatment cycle. Treatment with PMSG on days 5,17 resulted in increased estrous cycle lengths in both cows (P<.05) and heifers (P<.10) compared to a single treatment on day 17. The number of corpora lutea observed at laparotomy 7 to 11 days after estrus was greater in cows on Trt 17 than in cows on Trt 5, 17 (P<.10), but was similar in both heifer groups (P>.25). Plasma progesterone concentrations were similar in both groups prior to treatment but increased after day 5 in Trt 5, 17 compared to Trt 17 (P<.005). Plasma progesterone at time of laparotomy was significantly correlated with the number of corpora lutea (r = .75, P<.01). Plasma estradiol also increased after day 5 in Trt 5, 17 (P<.025). Estradiol was similar in both groups on day 17; but on day 19, cows on Trt 17 had greater plasma estradiol (P<.025) than cows on Trt 5, 17. Similarly, plasma estradiol concentrations for heifers treated only once were greater on day 19 than for heifers treated on days 5 and 17 (P<.05). Plasma LH concentrations were not significantly different between the two treatments. These results indicate the PMSG alters ovarian function when given either late in the luteal phase or during both early and late luteal phases of the estrous cycle.
1 Journal Article 3545 of the Agr. Exp. Sta. Oklahoma State Univ., Stillwater. This research was conducted in cooperation with the USDA, SEA.
2 We thank Dr. J. V. Whiteman and Dr. D. C. Meyerhoeffer for technical assistance in this study. We also thank Dr. G. D. Niswender (Department of Physiology and Biophysics, Colorado State Univ., Fort Collins) for the Progesterone-6β-BSA (No. 869), 17β-estradiol-6β-BSA (No. 244) and bovine LH (B225) antisera; Dr. L. E. Reichert, Jr. (Department of Biochemistry, Emory Univ. School of Medicine, Atlanta, GA) for the supply of bovine LH for iodination; the National Institute of Arthritis, Metabolism and Digestive Diseases for the supply of LH standard (NIH-LH-B8); and the Division of Biological Standards, National Institute for Medical Research, Hampstead Laboratories, Holly Hill, London for the PMSG standard.
3 Present address: Dept. of Animal and Range Sciences, New Mexico State Univ., Las Cruces 88003.
5 Present address: Department of Obstetrics and Gynecology, Univ. of Alabama in Birmingham, Univ. Station, Birmingham 35294.
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