A study was conducted to determine the effects of pregnancy-specific protein B (PSPB) and prostaglandin F2 alpha (PGF2 alpha) on bovine luteal cell progesterone, prostaglandin E2 (PGE2) and oxytocin production in vitro. Corpora lutea were enucleated from multiparous cows with normal oestrous cycles during the mid-luteal (days 10-12; n = 5) or late-luteal (days 17-18; n = 5) stage. Mixed large and small cells (1.5 x 10(5) cells per well) were incubated in 500 microliters modified Ham's F-12 medium. Cells were incubated for 18 h before treatments were added. Cells were treated with PSPB (0, 2.5, 5.0 micrograms) and PGF2 alpha (0, 100, 200 ng) in a 3 x 3 factorial arrangement. After treatments were added, media samples were collected at 6 and 12 h. During the 18 h pretreatment incubation, progesterone, PGE2 and oxytocin production was similar between the prospective treatment groups. Progesterone production was greater (P < 0.001) by mid-stage than by late-stage cells. In addition, progesterone decreased (P < 0.001) as incubation time increased. Progesterone production was not affected by PGF2 alpha, but PSPB increased (P < 0.02) progesterone at the 5.0 micrograms dose. Late-stage luteal cells produced more (P < 0.001) PGE2 than did mid-stage cells; PGE2 production decreased (P < 0.001) with increased incubation time. Luteal PGE2 production increased in response to PSPB treatment (P < 0.01) and PGF2 alpha treatment (P < 0.001). Luteal oxytocin production was greater (P < 0.01) by mid-stage compared with late-stage cells. Oxytocin production decreased (P < 0.001) with incubation time in mid-stage cells, but in late-stage cells oxytocin production was similar over time. Neither PSPB nor PGF2 alpha had an effect on oxytocin. These results indicate that PSPB does not affect luteal oxytocin, but does increase progesterone and PGE2 production. In addition, PGF2 alpha increases luteal PGE2, but does not affect progesterone or oxytocin production. These data do not show an interaction between PSPB and PGF2 alpha in regulating bovine luteal cell endocrine function.

R. 2001. The effects of gonadotrophin releasing hormone in prostaglandin F 2α α -based timed insemination programs for beef cattle. Can. J. Anim. Sci. 81: 335-343. Trials were conducted in the spring (May; n = 324) and fall (October; n = 132) with crossbred continental-type beef cows assigned on the basis of parity and postpartum interval to one of three timed-AI treatments and one of two post-AI treatments. The timed-AI treatments were: (DPG) double (14 d apart) PGF 2α (Lutalyse ® ) and AI (day = 0) 72 h after the second PGF 2α (day -3); (OVS) Ovsynch ® with the second GnRH (Factrel ® ) at 48 h and AI at 66 h; and (BRC) the same as OVS except that the second GnRH was given at the time of AI. Half of the cows within each treatment were given GnRH on day 14. Plasma progesterone concentrations were determined for the day of the first injection and on days -3, 0, 14, and 21. Timed-AI pregnancy was diagnosed by ultrasonography at day 42 and confirmed at calving. For DPG, OVS and BRC, PGF 2α responder rates were 75.9, 51.4 and 71.3%, respectively, in spring (P < 0.05) and 70.4, 70.4 and 59.1% in fall (P > 0.05), and AI pregnancy rates were 28.7, 44.9 and 44.4% in spring (P < 0.05) and 25.0, 40.9 and 43.2% in fall (P > 0.05). Post-AI GnRH had no significant effect on pregnancy or conception rates or day 21 progesterone. The use of GnRH in the PGF 2α based timed-AI program improved pregnancy rates and the BRC treatment was as effective as OVS. Neither postpartum interval nor initial progesterone concentration influenced (P > 0.05) the effect of GnRH on AI pregnancy rate, and GnRH had no effect (P > 0.05) on twinning rate or gender ratio.

No abstract

This experiment examined production of prostaglandin (PG) F2alpha, PGE2 and progesterone by bovine luteal cells incubated with or without the accessory cells and treated with recombinant bovine interleukin-1beta (10 ng), indomethacin (5 microg) or luteinizing hormone (50 ng). During pretreatment, progesterone production was similar in the luteal and luteal plus accessory cells, being greater in either of these than in accessory cells; PGF2alpha was greatest in luteal plus accessory, intermediate in accessory and lowest in the luteal cells; PGE2 was similar among all cell arrangements. Luteinizing hormone or luteinizing hormone plus indomethacin stimulated progesterone in the luteal and luteal plus accessory cells, this being similar in these two cell arrangements. Interleukin-1beta stimulated PGF2alpha in luteal and luteal plus accessory cells, and tended to elevate PGF2alpha in accessory cells. Interleukin-1beta stimulated PGE2 in all cell arrangements. Indomethacin inhibited the interleukin-1beta-stimulated PGF2alpha and PGE2 release. Indomethacin or indomethacin plus luteinizing hormone inhibited basal PGE2 in luteal and luteal plus accessory cells. These data suggest that progesterone production is not influenced by the presence of accessory cells of the corpus luteum, that accessory and luteal cells produce appreciable amounts of PG, and that recombinant bovine interleukin-1beta stimulates PGE2 and PGF2alpha in the luteal and accessory cells.