Ovulatory follicle dysfunction in lactating dairy cows after treatment with Folltropin-V at the onset of luteolysis.

The objective was to examine growth of the ovulatory follicle after FSH (Folltropin-V; Bioniche Animal Health, Belleville, Ontario, Canada) was given at the onset of induced luteolysis during a synchronization of ovulation protocol. Using GnRH or hCG for inducing ovulation enabled assessing ovulatory follicle responsiveness to an endogenous versus exogenous surge of LH activity. At 8 to 10 days after estrus (synchronized estrus = Day 0), lactating dairy cows received an Eazi-Breed CIDR (Pfizer Animal Health) plus 100 µg GnRH. After 7 days, controlled internal drug release devices (CIDRs) were removed, cows were given 500 µg cloprostenol, and then randomly allocated to receive 80 mg Folltropin-V (FSH; N = 19) or 4 mL sterile saline (SAL; N = 16). After 49 hours, FSH and SAL cows were randomly allocated to receive 100 µg GnRH or 3000 IU hCG. Five cows ovulated 30 to 42 hours (38.4 ± 1.2 hours) after FSH treatment. In the remaining FSH (N = 14) or SAL (N = 16) cows, ovulatory follicle size was similar at CIDR removal (14.5 ± 0.6 and 14.7 ± 0.6 mm, respectively; P = 0.85) and when GnRH/hCG was given (16.6 ± 0.6 and 17.7 ± 0.6 mm, respectively; P = 0.23). Estradiol-17ß concentrations were lower in FSH cows at 36 and 49 hours after CIDR removal (FSH by time interaction, P < 0.005). After GnRH or hCG treatment, four FSH cows failed to ovulate. In cows exhibiting ovulation, the last recorded size of the ovulatory follicle was not influenced by FSH (18.1 ± 0.9 and 17.5 ± 0.6 mm for FSH and SAL, respectively; P = 0.59) or hormonal induction approach (18.4 ± 0.9 and 17.2 ± 0.7 mm for GnRH and hCG, respectively; P = 0.29). The interval from onset of luteolysis to ovulation and pharmaceutical induction to ovulation was shorter in FSH cows given GnRH (FSH by pharmaceutical inducer [GnRH vs. hCG] interaction; P = 0.01). Cows receiving GnRH had an LH surge; hCG-treated cows did not. Maximum LH concentrations were greater (P < 0.04) in SAL versus FSH cows after GnRH treatment (10.9 ± 1.2 vs. 6.7 ± 1.4 ng/mL, respectively). In three FSH cows failing to ovulate after GnRH treatment, the maximum LH concentration was <4 ng/mL. When analyzed from GnRH treatment, average time to LH maximum concentration was similar (P = 0.50) to values obtained in cows receiving FSH and GnRH and SAL and GnRH (1.7 ± 0.2 vs. 1.9 ± 0.1 hours, respectively). Interval to maximum hCG concentrations was shorter (P = 0.02) for cows receiving SAL versus FSH (8.0 ± 0.8 and 10.0 ± 0.8 hours for SAL and FSH, respectively). Ovulatory dysfunction of this magnitude highlighted the lack of suitability of Folltropin-V at a dose of 80 mg at the time of induction of luteolysis in fixed timed AI protocols.

Influence of a prostaglandin synthesis inhibitor administered at embryo transfer on pregnancy rates of recipient cows.

Elevated uterine luminal concentrations of prostaglandin F(2alpha) (PGF(2alpha)) have been negatively associated with embryo quality and pregnancy rates. Two studies were performed in cows to determine PGF(2alpha) release from uterine endometrium following embryo transfer and to investigate administration of flunixin meglumine (FM), a prostaglandin synthesis inhibitor, on pregnancy rates following embryo transfer. In Experiment 1, blood samples were collected prior to and after embryo transfer from the posterior vena cava via saphenous vein cannulation. Serum profiles of PGF(2alpha) indicated that manipulation of the reproductive tract during embryo transfer was followed by increased release of PGF(2alpha) from the uterine endometrium. In Experiment 2, estrus (day=0) was synchronized in recipient animals and a single embryo transferred 7 days after estrus. At the time of non-surgical embryo transfer, animals were randomly assigned to receive either FM (FM; n=1300) or remain untreated (control (CON); n=797). Data collected at transfer included stage of embryo development, embryo quality, technician, and transfer quality score. Overall pregnancy rates of cows receiving FM (65%) were higher than control cows (60%; P<0.02). Pregnancy rates following transfer of quality 1 (good) embryos did not differ (P>0.05) between treatments. However, pregnancy rates of quality 2 (fair) embryos were higher in animals receiving FM than in CON (P<0.01). Moreover, pregnancy rates of transferred morula- and blastocyst-stage embryos were higher in FM-treated than in controls (P<0.06 and P<0.04, respectively). In conclusion, uterine release of PGF(2alpha) is elevated following embryo transfer and administration of a PGF(2alpha) synthesis inhibitor at the time of embryo transfer improved pregnancy rates in cows.

Effects of induced clinical mastitis during preovulation on endocrine and follicular function.

The objective of the study was to determine if experimentally induced clinical mastitis before ovulation resulted in alterations of endocrine function, follicular growth, or ovulation. On d 8 (estrus = d 0), cows were challenged (TRT; n = 19) with Streptococcus uberis or were not challenged (control; n = 14). Forty-eight hours after induction of luteal regression on d 12, blood samples were collected to determine estradiol-17beta, LH pulse frequency, and occurrence of the LH surge. Ovaries were scanned to monitor follicular growth and ovulation. Cows with clinical mastitis (n = 12) had elevated rectal temperatures, somatic cell counts, and mammary scores. Estrus and ovulation occurred in 4 of 12 clinically infected cows and in all control cows. Cows that were challenged but did not develop clinical mastitis (n = 5) displayed estrus and ovulated. Due to differences in expression of estrus, cows were further subdivided for analyses into 4 groups: control, TRT-EST (infected cows that displayed estrus; n = 4), TRT-NOEST (infected cows that did not display estrus; n = 8), and NOMAS (cows that were inoculated but did not develop mastitis; n = 4). Ovulation rate was 100% for CON, NOMAS, and TRT-EST compared with 0% for TRT-NOEST cows. Size of the ovulatory follicle ("presumed" ovulatory follicle in TRT-NOEST cows) was similar for all groups. Frequency of LH pulses was decreased in TRT-NOEST compared with CON, TRT-EST, and NO-MAS. Estradiol-17beta increased over time in CON, NO-MAS, and TRT-EST cows, but did not increase in TRT-NOEST cows. Cows with clinical mastitis may exhibit estrus and ovulate normally or have disruptions in normal physiology including decreased LH pulsatility, absence of an LH surge and estrous behavior, suppressed estradiol-17beta, and failure to ovulate.

Fertility aspects in yearling beef bulls grazing endophyte-infected tall fescue pastures.

During a 2-year study, yearling beef bulls were used to determine the effects of grazing on endophyte-infected tall fescue on endocrine profiles, semen quality and fertilisation potential. Bulls were allotted to graze tall fescue pastures infected with Neotyphodium coenophialum (E+; n = 20 per year) or Jesup/MaxQ (Pennington Seed, Atlanta, GA, USA; NTE; n = 10 per year). Bulls were grouped by scrotal circumference (SC), bodyweight (BW), breed composites and age to graze tall fescue pastures from mid-November until the end of June (within each year). Blood samples, BW, SC and rectal temperatures (RT) were collected every 14 days. Semen was collected from bulls every 60 days by electroejaculation and evaluated for motility and morphology. The developmental competence of oocytes fertilised in vitro with semen from respective treatments was determined. Bulls grazing E+ pastures had decreased BW gain (P < 0.01), increased overall RT (P < 0.01) and decreased prolactin (P < 0.01) compared with animals grazing NTE pastures. Neither percentage of normal sperm morphology nor motility differed between bulls grazed on the two pasture types. Semen from E+ bulls demonstrated decreased cleavage rates (P = 0.02) compared with semen from NTE bulls. However, development of cleaved embryos to the eight-cell and blastocyst stages did not differ between the two groups. In conclusion, semen from bulls grazing E+ tall fescue resulted in decreased cleavage rates in vitro, which may lower reproductive performance owing to reduced fertilisation ability.

Detrimental effects of prostaglandin F2alpha on preimplantation bovine embryos.

Two studies were performed to determine effects of prostaglandin F2alpha (PGF2alpha) on continued development of pre-compacted (in vitro-produced) and compacted (in vivo-derived) bovine embryos. In Experiment 1, pre-compacted embryos were placed in KSOM media supplemented with polyvinyl alcohol (0.3%) and assigned to the following treatments: (1) control; (2) PGF-1 (1 ng/mL PGF2alpha); (3) PGF-10 (10 ng/mL PGF2alpha); (4) PGF-100 (l00 ng/mL PGF2alpha); or (5) PGE-5 (5 ng/mL PGE2). Following 4 days of incubation in assigned treatments, continued development of pre-compacted embryos to blastocysts was reduced by addition of PGF2alpha in culture medium (P = 0.002). Development did not differ between control and PGE2 treatments (P > 0.10). In Experiment 2, compacted morula' s were placed in KSOM-PVA supplemented media and assigned to one of four treatments: (1) control; (2) PGF-0.1 (0.1 ng/mL PGF2alpha); (3) PGF-1 (1 ng/mL PGF2alpha); and (4) PGF-10 (10 ng/mL PGF2alpha). After 24h in culture, embryos were washed and placed in KSOM-BSA (0.5%) without PGF2alpha for an additional 48 h until assessment for development. Continued development of compacted morula to blastocyst was not affected by addition of PGF2alpha to the culture medium (P > 0.10). However, hatching rates of embryos cultured with PGF2alpha were lower (P = 0.05). In conclusion, it is suggested that PGF2alpha has a direct negative effect on continued embryonic development of pre-compacted and compacted bovine embryos.

Alterations in embryo development in progestogen-supplemented cows administered prostaglandin F2alpha.

The objective was to examine effects of elevated prostaglandin F2alpha (PGF) on embryo development in cows supplemented with exogenous progestogen. Cows were artificially inseminated at estrus (Day 0) and a synthetic progestogen supplemented in the feed from Days 3 to 8. Cows were allotted randomly to receive either 15 mg PGF (TRT) or saline (CON) at 06:00, 14:00 and 22:00 h from Days 5 to 8. Blood samples were collected at 06:00 and 22:00 h from Days 5 to 8 for determination of progesterone and 13,14-dihydro-15-keto-PGF2alpha (PGFM). Single embryos were recovered on Day 8, assigned a quality score, and stage of development recorded. Progesterone was lower from Days 5 to 8 in TRT versus CON cows (P = 0.0001). Concentrations of PGFM from Days 5 to 8 were elevated in TRT compared to CON cows (P = 0.0001). Embryo quality was reduced in TRT cows compared to CON cows (P = 0.059). Percentage of embryos considered transferable was decreased by administration of PGF (P = 0.003). Sixty-four percent of TRT embryos were retarded in development at Day 8, whereas 80% of CON embryos had developed to expanded blastocysts (P = 0.003). In conclusion, treatment of progestogen-supplemented cows with PGF reduced quality and retarded development of embryos. Decreased fertility in conditions causing elevated concentrations of PGF may result from altered embryo development and quality.