Estrógeno e prostaglandina F2 alfa no controle de funções reprodutivas em fêmeas bovinas

Abstract

The reproductive efficiency has repercussion on productivity and profitability of cattle industry and can be influenced by several factors, as uterine disorders and the efficiency of estrous cycle manipulation and ovulation. In the first study, we reviewed and discussed the aspects regarding the estrogen exposure to prevent or treat reproductive disorders, focusing on the uterine environment. Based on this review, we concluded that the estrogen has an important role in the uterine environment; nevertheless, it did not exhibit beneficial effects to treat or prevent uterine disorders when used in isolated doses. However, when repeat breeding cows were submitted to estrogen of long exposure in protocols of artificial induction of lactation, we observed beneficial effects on reproductive performance in these animals, being important to investigate, in a controlled manner, the effect of estrogen on fertility. Subsequently, given that the manipulation of estrous cycle and ovulation induction are essential to the Fixed-Time Artificial Insemination protocols (FTAI), it was demonstrated that the prostaglandin F2α (PGF) is important in the ovulation process, though the precise mechanism of action has not been elucidated, making the validation of an in vivo model for studying the function of prostaglandins in ovulation considerable. In this respect, in the second study we aimed to: assess the effect of the nonsteroidal anti-inflammatory drug (NSAID) Flunixin Meglumine (FM; 2,2 mg/Kg), a cyclooxygenase inhibitor, on the concentrations of PGF and its metabolite (13,14-di-hydro-15-ceto-PGF, PGFM) in the follicular fluid; to confirm whether the parenteral administration of PGF analogous (dinoprost tromethamine; 25 mg) would be able to alter the intra-follicular concentrations of PGF and PGFM; and to assess the effect of the NSAID FM on ovulation and subsequent luteal function. For that, cyclical Jersey cows (n = 18) were submitted to an estrus synchronization protocol, and, after the application of GnRH, were allocated in three groups, according to the follicular diameter (>11 mm): CONTROL (n = 6), untreated; NSAID FM (n = 6), who received an FM application 17 h after GnRH; and NSAID FM + PGF (n = 6), in which FM was administered 17 h after GnRH and PGF 23 h after GnRH. The FF was collected 24 h after GnRH, with a higher concentration of PGFM in the NSAID FM + PGF group and a higher concentration of PGF in the CONTROL group (P <0.01). To assess ovulation and luteal function, cyclical Jersey cows (n = 19) were synchronized and, after the application of GnRH, distributed into two groups, according to the follicular diameter (>11 mm): CONTROL (n = 10), untreated; and NSAID FM (n = 9), submitted to a dose of FM 17 h after GnRH. Follicles were followed up to 42 h after GnRH and blood collection for progesterone measurement was performed five days after GnRH, all control animals and six animals of the NSAID FM ovulated up to 42 h after GnRH and serum progesterone concentrations did not differ between groups (P> 0.05). Based on our findings, it is possible to concluded that the FM inhibited PGF synthesis within the follicle and the parenteral administration of PGF did not alter the intra-follicular concentrations of PGF. The administration of a single dose of FM in the final phase of the ovulatory process did not affect the ovulation and the subsequent synthesis of progesterone by the corpus luteum. On the other hand, it is necessary to test other NSAIDs to stablish a systemic model of ovulation inhibition in order to investigate the function of prostaglandins in this process.