Infertility associated with the duration of luteal phase in postpartum cows

After first postpartum ovulation most cows have a short luteal phase due to a premature secretion of PGF2 from the uterus. Pregnancy rate in estrous cycles with short luteal phases is essentially nil. The lack of exposure of the uterus to P4 and estrogen prior to first postpartum ovulation decreases the concentration of P4 receptors and up regulates oxytocin receptors. The inadequate number of P4 receptors and presence of endometrial oxytocin receptors earlier in cows with short than normal luteal phases allows premature release of PGF2a and the resultant regression of the CL. During luteolysis, uterine and luteal PGF2a cause death of the embryos mainly during the transition from morula to blastocyst when the embryos are more susceptible to embryotoxic effect

Infertilidad asociada con la duración de la fase luteal en vacas postparto

After first postpartum ovulation most cows have a short luteal phase due to a premature secretion of PGF2α from the uterus. Pregnancy rate in estrous cycles with short luteal phases is essentially nil. The lack of exposure of the uterus to P4 and estrogen prior to first postpartum ovulation decreases the concentration of P4 receptors and up regulates oxytocin receptors. The inadequate number of P4 receptors and presence of endometrial oxytocin receptors earlier in cows with short than normal luteal phases allows premature release of PGF2α and the resultant regression of the CL. During luteolysis, uterine and luteal PGF2α cause death of the embryos mainly during the transition from morula to blastocyst when the embryos are more susceptible to embryotoxic effect

Induction of Estrus in Anestrous Suckled Beef Cows

Suckled anestrous beef cows (n=362) received either: 1) an intravaginal implant containing progesterone for 7 days plus a 1 mg injection of estradiol benzoate 24 to 30 hours after implant removal; 2) an intravaginal implant containing progesterone for 7 days; 3) a sham implant for 7 days plus a 1 mg injection of estradiol benzoate 24 to 30 hours after implant removal; or 4) a sham implant for 7 days. Treatment with progesterone resulted in resumption of luteal function in suckled anestrous beef cows with most cows developing corpora lutea with a typical lifespan, whereas treatment with estradiol benzoate enhanced the expression of estrus

Developmental Programming: Exogenous Gonadotropin Treatment Rescues Ovulatory Function But Does Not Completely Normalize Ovarian Function in Sheep Treated Prenatally with Testosterone1

Prenatal testosterone treatment leads to LH excess as well as ovarian follicular and ovulatory defects in the adult. These disruptions may stem from LH excess, abnormal FSH input, compromised ovarian sensitivity to gonadotropins, or intrinsic ovarian defects. To determine if exogenous gonadotropins rescue ovarian and ovulatory function of testosterone-treated sheep, the release of endogenous LH and biopotent FSH in control and prenatal testosterone-treated sheep was blocked with a GnRH antagonist during the first two breeding seasons and with LH/FSH coadministered in a manner approximating natural follicular phase. An acidic mix of FSH was administered the first 36 h at 2-h intervals and a less acidic mix for the next 12 h at 1-h intervals (different FSH preparations were used each year), and ovulation was induced with hCG. Circulating FSH and estradiol responses to gonadotropins measured in 2-h samples differed between treatment groups in Year 1 but not in Year 2. Ovarian follicular distribution and number of corpora lutea (in ewes that ovulated) tracked by ultrasonography and luteal progesterone responses were similar between control and prenatal testosterone-treated females but differed between years. Furthermore, hCG administration induced large cystic and luteinized follicles in both groups of females in Year 2, although the growth rate differed between control and prenatal testosterone-treated females. Our findings provide evidence that 1) ovulatory response in prenatal testosterone-treated females can be rescued with exogenous gonadotropins, 2) resultant follicular response is dependent on the nature of gonadotropic input, and 3) an abnormal follicular milieu may underlie differences in developmental trajectory of cystic follicles in prenatal testosterone-treated females