FACTORS AFFECTING FERTILITY IN THE POSTPARTUM COW - ROLE OF THE OOCYTE AND FOLLICLE IN CONCEPTION RATE

Four experiments were designed to examine the contribution of the oocyte or the follicular, oviductal, or early uterine environments to low fertility associated with the first ovulation postpartum. At 17-25 days postpartum in experiments 1, 2, and 3, suckled beef cows were assigned at random to receive 6 mg norgestomet, via ear-implant, for 9 days (NOR) or to serve as controls (CON). Calves were weaned from all cows 7 days after assignment to treatment in order to induce estrus, an LH surge, ovulation, and subsequent formation of CL. As cows were detected to be in estrus, they were bred first by natural service and 12 h later by artificial insemination. In experiment 1, on Day 3 after estrus, the oviduct ipsilateral to the side of ovulation was removed and flushed for recovery of an embryo or oocyte. Rates of recovery (86%), fertilization (68%), and development of fertilized oocytes to the 4- to 8-cell stage (100%) did not differ between CON and NOR cows. In experiment 2, uteri were flushed nonsurgically on Day 6 after estrus. Rates of recovery of embryos from the uterus were similar between CON (86%) and NOR (71%) cows. In experiment 3, one half of the cows in each group (CON and NOR) were fed melengestrol acetate (MGA) beginning on Day 4 after estrus and continuing until Day 35. The remaining cows in each group served as controls. Treatment with NOR increased (p < 0.05) the proportion of cows that maintained pregnancy until Day 35 (9/22) as compared to controls (0/18). Supplementation with MGA failed to improve maintenance of pregnancy in cows that underwent early luteal regression. In experiment 4 progesterone (200 mg/day) was injected, beginning on Day 4 after cows were bred at first postpartum estrus, to produce luteal-phase concentrations in circulation. This treatment also failed to maintain pregnancy in CON cows with short-lived CL In conclusion, low pregnancy rate in CON cows was due not only to premature regression of the CL; it may have resulted from ovulation of an oocyte with inherent or acquired defects preventing continued development, or from an oviductal or uterine environment hostile to the developing embryo.