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during Blockade of Luteolysis in Pigs after human Chorionic Gonadotropin Treatment1,2,US Department of Agriculture3, Beltsville, MD 20705
Abstract
An injection of human chorionic gonadotropin (HCG) or estrogen on d 12 of the estrous cycle delays luteolysis in the pig. In an experiment to determine if HCG stimulated estrogen secretion, 21 cyclic pigs received one of five different amounts of HCG-(A) 0, (B) 125, (C) 250, (D) 500 or (E) 1,000 IU-as a single, im injection in 2 ml of distilled water on d 12 of the estrous cycle. Blood was collected from the jugular vein immediately before HCG injection and once daily thereafter until d 20 of the estrous cycle. Plasma progesterone, estrogen (unconjugated) and 13,14-dihyro-15-keto-pros-taglandin F2
(PGFM) were quantified for pigs in all groups; luteinizing hormone (LH) and follicle stimulating hormone (FSH) were quantified for pigs in groups A and E. The HCG injection exerted a dose related increase on the mean interestrus interval (groups A, B, C, D and E were 20.5, 20.2, 22.5, 31.0 and 61.4 d, respectively) and on the delay of luteolysis as measured by mean plasma progesterone on d 16 (A, B and C vs D and E, respectively, 1.9, 1.2 and 10.4 vs 34.1 and 47.1 ng/ml; P<.05). The HCG injection caused a transitory increase in plasma estrogen from d 12 (5 to 10 pg/ml before treatment) to d 15 (35.5 pg/ml, group D) and to d 16 (90.2 pg/ml, group E) before it decreased to preinjection levels on d 17 (group D) and 18 (group E). No preovulatory surge of LH or FSH was detected for pigs in group E; plasma LH and FSH were depressed compared with group A (P<.05). In contrast, in groups A and B, plasma estrogen peaked on d 19 and culminated in preovulatory LH and FSH surges on d 20 in group A. The late luteal phase increases in plasma PGFM typical of cyclic pigs were present in pigs of groups A and B; these increases in plasma PGFM were absent in pigs of group E. Data are consistent with the hypothesis that injection of HCG stimulated follicular estrogen production and secretion.
1 The authors thank Dr. L. Reichert, Jr., National Pituitary Agency and the USDA Hormone Program for purified pituitary hormones; Drs. G. Niswender and K. Kirton for antisera, and Dr. J. Pike for prostaglandins used in this study. The authors wish to thank Kathy Yeager and Rosemary Rollins for technical assistance.
2 Mention of a trade name, proprietary product or specific equipment does not constitute a guarantee or warranty by the USDA and does not imply its approval to the exclusion of other products that may be suitable.
3 Reproduction Laboratory, Anim. Sci. Institute, ARS.
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