|Cushman, Robert - Bob|
Submitted to: Journal of Animal Science
Publication Type: Peer reviewed journal
Publication Acceptance Date: 4/27/1999
Publication Date: N/A
Citation: Cushman, R.A., Davis, P.E., Boonyaprakob, U., Hedgpeth, V.S., Burns, P.J., Britt, J.H. 1999. Technical note: Use of slow-release estradiol and prostaglandin F2alpha to induce pseudopregnancy and control estrus in gilts. Journal of Animal Science. 77(11):2883-2885. Interpretive Summary: Unlike cows and sheep, pigs are not responsive to prostaglandin to synchronize estrus until late in the estrous cycle, making prostglandins ineffective in this species because they will enter estrus naturally. Estrogens have been used to induce maintenance of the corpus luteum (CL, pseudoepregnancy) as a method to generate pools of gilts with prostaglandin-sensitive CL that can be synchronized upon entry into the breeding barn. However, the number of estrogen shots required makes this method ineffective. We determined whether a single injection of a slow-release estrogen (SRE) would induce pseudopregnancy in gilts and whether PGF2alpha would regress the corpora lutea of pseudopregnancy. Gilts were induced to ovulate with PG600 at 180 d of age, and 14 days later, gilts were injected i.m. with one of five doses of SRE (0, 12.5, 25, 50, or 100 mg). After 59 days, gilts received 10 mg of PGF2alpha, and were checked for estrus for 7 d. Treatment with SRE increased duration of luteal function. There were no differences among doses of SRE in the percentage of pseudopregnant gilts that showed estrus after PGF2alpha. We conclude that a single injection of SRE can induce pseudopregnancy and that the CL can be regressed with PGF2alpha, providing a simple method for controlling estrus in gilts.
Technical Abstract: We determined whether a single injection of slow-release estradiol-17beta (SRE2) would induce pseudopregnancy in gilts and whether PGF2alpha would regress the corpora lutea (CL) of pseudopregnancy. Crossbred gilts (n = 40) were induced to ovulate by treatment with 400 IU of hCG + 200 IU of eCG (PG600, Intervet, Millsboro, DE) given at 180 d of age (d = 0). On d 14, gilts were injected i.m. with one of five doses (n = 8 gilts/dose) of SRE2 (0, 12.5, 25, 50, or 100 mg). Blood samples were collected before SRE2 and twice weekly until d 73 to monitor serum progesterone (P4) and estradiol (E2). On d 59, gilts received (i.m.) 10 m of PGF2alpha (Lutalyse, Pharmacia Upjohn, Kalamazoo, MI) and were checked for estrus for 7 d. On d 62, mammary development was scored (0 = no development; 1 = some development; 2 = teat and gland development) by a neutral observer. Treatment with SRE2 increased (P < .05) peak E2 concentrations, duration of luteal function, and mammary gland score. There were no differences (chi-square, P > .05) among doses of SRE2 in the percentage of pseudopregnant gilts that showed luteolysis after PGF2alpha. We conclude that a single injection of SRE2 can induce pseudopregnancy and that the CL can be regressed with PGF2alpha, providing a simple method for controlling estrus in gilts.