P. L. Wolfe

Effect of 17β-estradiol on the preovulatory surge of LH in the bovine female☆

The hypothesis tested was that increasing concentration of 17beta-estradiol (E(2)) subsequent to luteolysis stimulates the preovulatory surge of LH and that a decline in E(2) after the initial rise is not necessary to trigger the preovulatory surge of LH in the bovine female. Beef cows were synchronized to Day 16 of the estrous cycle. At Hour 0, all cows were ovariectomized and received one of four E(2) treatments: 1) luteal phase E(2) (LE; n=5), 2) increasing then decreasing E(2) (DE; n=5), 3) increasing and subsequent maintenance of high E(2) (IE; n=4), and 4) no E(2) (NE; n=3). Cows in the LE group received one E(2) implant at Hour 0 which provided low concentrations of E(2). Cows in the DE group received one E(2) implant at 0, 8, 16, 24, 32 and 40 hours; implants were subsequently removed at 8-hour intervals, thus mimicking the preovulatory rise and fall of E(2). Cows in the IE group were treated with the same regimen of E(2) implants as cows of the DE group, except that no E(2) implants were removed. Blood samples were collected at Hour 0 and at hourly intervals from Hour 2 through 80, for serum LH and E(2) quantification. The number of cows responding with a surge of LH was 0/3, 0/5, 4/5 and 3/4 for the NE, LE, DE and IE treatments, respectively. The proportion of cows responding with an LH surge was different (P<0.01) when data for cows in the NE and LE groups were pooled and compared with the pooled data of cows in the DE and IE groups. The mean time of the LH surge was not different (P>0.80) for cows responding with an LH surge (DE and IE treatments). Thus, increased levels of E(2) greater than luteal phase concentrations are needed to initiate preovulatory surges of LH, and it appears that concentrations of E(2) need to reach a certain level but do not need to decrease after this initial rise to stimulate a surge release of LH.

Luteinizing hormone and progesterone concentrations in serum of heifers administered a short half-life prostaglandin (PGF2α) or long half-life prostaglandin analogue (fenprostalene) on days six or eleven of the estrous cycle☆

Two trials were conducted to measure the progesterone (P(4)) decline and luteinizing hormone (LH) surge in serum subsequent to administration of a short half-life (short t (1 2 )) prostaglandin (PGF(2alpha)) or a long half-life (long t (1 2 )) prostaglandin analogue (fenprostalene) on Days 6 or 11 of the estrous cycle. Twenty-five crossbred Shorthorn and five Hereford heifers with a mean weight of 331.4 +/- 29.8 kg were used in both trials. The heifers were randomly allotted to receive either a short t (1 2 ) or long t (1 2 ) prostaglandin treatment on Day 6 or 11 of the estrous cycle. A crossover design for the main effect, treatment (type of prostaglandin), was conducted. Heifers that received PGF(2alpha) in Trial I were given fenprostalene in Trial II and vice versa. Stage of the estrous cycle (day) was the same for each heifer in both trials. Stage of estrous cycle was standardized to either Day 6 or 11 by administering Syncro-Mate B (SMB). Blood was collected every hour for 80 h post injection to quantify LH and P(4) concentrations. There were no significant differences (P > 0.05) between the short t (1 2 ) or long t (1 2 ) for either P(4) or LH profiles. In addition, no differences were detected between stages of the estrous cycle for the timing of the preovulatory surge of LH after prostaglandin administration.

Response to luteinizing hormone releasing hormone in postpubertal boars with large testes

The objective of the present study was to determine if postpubertal boars (12-13 months of age; 156 +/- 8 kg) with large testes had altered hypothalamic control of secretion of luteinizing hormone (LH). Seven boars with the highest estimated 150 d, paired testis weights from a line selected for large testes (769 +/- 60 g = mean weight of excised testes) and 8 boars from a control group (control, 544 +/- 20 g) were tethered in stalls and fitted with indwelling jugular catheters. Males were bled when they were intact, 14 days after castration and during administration of sodium pentobarbital anesthetic (subsequent to castration) to block secretion of endogenous LH-releasing hormone (LHRH). Blood samples were collected at 12-min intervals for 6 hr before and 1 hr after intravenous injection of LHRH in intact and castrated males. During anesthesia, LHRH was administered 4 times at 1-hr intervals and blood samples were collected every 6 min. All samples were analyzed for concentrations of LH and pooled samples were analyzed for concentrations of 17-beta estradiol (E2) and testosterone (T). In intact and castrated males, mean concentrations of LH, frequency and amplitude of pulses of LH, and concentrations of E2 and T were not different between boars of the two groups (P greater than .10). Response to exogenous LHRH was less (P less than .05) in intact males with large testes than in corresponding males from the control group (P less than .05). Fourteen days after castration, males that had larger testes before castration had less of a response to LHRH than males from the control group (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)