Efficacy of either a single or split treatment of PGF2α after a 14 day melengestrol acetate treatment to synchronize estrus and induce luteolysis in Bos indicus × Bos taurus heifers

Two experiments evaluated a modified delivery of prostaglandin F2α (PGF2α) after a melengestrol acetate (MGA) treatment in Angus and Bos indicus × Bos taurus (BI) heifers. Experiment 1 was replicated three times with yearling BI heifers (n = 695). Heifers received MGA (0.5 mg head−1 day−1) for 14 days. In Replications 1 and 2, heifers received either 25 mg of PGF2α im 19 days after MGA (single) or 12.5 mg of PGF2α im 19 and 20 days after MGA (split). In Replication 3, heifers received the same treatments, with PGF2α initiated either 18 or 19 days after MGA. Estrus was detected for 72 h after PGF2α, with AI commencing 8-12 h after a detected estrus. Heifers not observed in estrus by 72 h were timed-AI concomitant with GnRH (100 μg im). Heifers from Replication 2 (n = 146) had blood samples collected at the initial PGF2α and at timed-AI to determine corpus luteum (CL) regression by evaluating plasma progesterone concentrations. The interval from MGA withdrawal to PGF2α did not have a significant effect on any variable in Replication 3 and there were no treatment by replication effects for any variables, therefore data were pooled. Modifying the PGF2α treatment from a single treatment to two treatments on consecutive days increased (P < 0.05) 72 h estrous response (43.2% versus 50.1%), timed-AI (23.9% versus 33.5%) and total-AI pregnancy rates (34.5% versus 42.5%), and CL regression (79.1% versus 92.5%), respectively. In Experiment 2, yearling Angus (n = 66) and 2-year-old BI (n = 68) heifers were synchronized as per Experiment 1 (with the initial PGF2α 19 days after MGA). Neither breed nor PGF2α treatment effected (P > 0.05) 72 h estrous response, total-AI pregnancy rate, or CL regression rate. In conclusion, treating yearling BI heifers with split treatments of PGF2α (given on two consecutive days) improved estrous response and pregnancy rates by increasing PGF2α-induced luteolysis.