Effects of P.G. 600 on the onset of estrus and ovulation rate in gilts treated with Regu-mate.

Three experiments assessed the onset of estrus and ovulation rate in gilts treated with gonadotropins after the withdrawal of an orally active progestin. In Exp. 1, all cycling gilts received the progestin (Regu-mate; Intervet America Inc., Millsboro, DE) at a rate of 15 mg/d for 18 d. Twenty-four hours after the last feeding of Regu-mate, 32 gilts received an i.m. injection of 400 I.U. PMSG and 200 I.U. hCG (P.G. 600, Intervet America, Inc.), and 32 gilts received an i.m. injection of deionized water. The percentage of gilts displaying estrus < or = 7 d (P = 0.64) and the injection-to-estrus interval (P = 0.37) were similar for P.G. 600-treated gilts (93.8% and 4.1 +/- 0.1 d) and controls (90.6% and 4.3 +/- 0.1 d). Ovulation rate was greater (P < 0.01) in P.G. 600-treated gilts (28.8 +/- 1.1) compared with controls (17.4 +/- 1.1). In Exp. 2, 58 cycling gilts received Regu-mate (15 mg/d) for 18 d. Twenty-four hours after Regu-mate withdrawal, gilts received i.m. P.G. 600 or water (n = 29/treatment). Gilts were bred via AI 12 and 24 h after first detection of estrus. The percentage of gilts displaying estrus < or = 7 d (P = 0.45) and the injection-to-estrus interval (P = 0.27) were similar for P.G. 600-treated gilts (82.7% and 4.0 +/- 0.1 d) and controls (89.7% and 4.2 +/- 0.1 d). Ovulation rate was greater (P < 0.01) in P.G. 600-treated gilts (26.2 +/- 1.8) compared with controls (18.1 +/- 1.7). Pregnancy rate (P = 0.71) and the number of live embryos at d 30 postmating (P = 0.40) were similar for P.G. 600-treated gilts (91.7% and 15.6 +/- 1.2) and controls (88.5% and 14.1 +/- 1.2). In Exp. 3, prepubertal gilts (142.6 +/- 0.7 d of age) received Regumate (15 mg/d) (n = 20) or a control diet not including Regu-mate (n = 20) for 18 d. Twenty-four hours after Regu-mate withdrawal, all gilts received i.m. P.G. 600. The percentage of gilts displaying estrus < or = 7 d (P = 0.49) and the P.G. 600-to-estrus interval (P = 0.69) were similar for Regu-mate-fed gilts (95% and 4.3 +/- 0.2 d) and controls (88.9% and 4.2 +/- 0.2 d). Ovulation rate was similar (P = 0.38) for Regu-mate fed gilts (16.6 +/-1.6) and controls (14.4 +/- 1.8). In cycling gilts, administration of P.G. 600 after withdrawal of Regu-mate increased ovulation rate, but not litter size at d 30 postmating. There was no beneficial effect of Regu-mate pretreatment on the response to P.G. 600 in prepubertal gilts.

Regression of induced corpora lutea in mature cyclic gilts by human chorionic gonadotropin.

This study was conducted to determine whether chronic hCG treatment would cause regression of induced corpora lutea (CL) in mature cyclic gilts. Thirty-two mature gilts that had displayed one or more estrous cycles of 18 to 22 d were used. Sixteen gilts were hysterectomized (HYSTX) on d 6 to 9 (d 0 = onset of estrus) and their CL were marked with charcoal (spontaneous group). Sixteen gilts (induced group) were injected with 1,500 IU of pregnant mare's serum gonadotropin (PMSG) on d 6 and 500 IU of hCG on d 9 (day of hCG = d 0 of the induced cycle). Ovulation was assumed to occur on d 2 of the induced cycle. Induced gilts were HYSTX on d 8 to 9 (d 17 to 18 of the original spontaneous cycle) and their CL were marked with charcoal. Only gilts (n = 14) in which induced CL were present and in which the original CL had regressed were then subjected to treatment with saline or hCG. From d 10 to 29, gilts with spontaneous CL were injected daily with 500 IU of hCG (n = 8) or saline (n = 8). From d 10 to 29 of the induced cycle, induced gilts were injected daily with 500 IU of hCG (n = 6) or saline (n = 8). Jugular blood samples were collected every other day from all gilts beginning on the 1st d of daily hCG treatment and quantified for estradiol and progesterone by RIA. On the day after the last hCG injection, the number of charcoal-marked CL and charcoal-marked corpora albicantia (CA) were determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Follicle growth in hypophysial stalk-transected pigs given pulsatile GnRH and pregnant mare serum gonadotropin.

In experiment 1, nine prepuberal crossbred gilts 145 +/- 2 days of age and 90.3 +/- 1.6 kg body weight (BW) were hypophysial stalk-transected (HST) or sham-HST. Starting at 0800 on Day 1 (35 +/- 2 days after surgery), three sham-HST and two HST gilts received 3.5% sodium citrate vehicle (V) while two HST gilts and two sham-HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 9 days via a jugular vein cannula. At 0800 on day 7, all gilts received 1,000 IU of pregnant mare serum gonadotropin (PMSG) im. Blood was sampled every 15 min from 0800 to 0845 on Days 1 through 6. On Day 10, ovarian morphology and ovarian and follicular fluid weights were recorded. In experiment 2, eight prepuberal crossbred gilts, 146 +/- 6 days of age and 79.5 +/- 1.5 kg BW, were HST or sham-HST. Starting at 0800 on Day 1 (7 +/- 4 days after surgery), two sham-HST and three HST gilts received V, while three HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 8 days. At 1200 on Day 5, all gilts, including three unoperated controls (UC), received 1,000 IU of PMSG im. Blood was sampled from all but UC gilts every 15 min from 0800 to 0845 on Days 1 through 5. Ovarian data were obtained on Day 9. The HST + V gilts failed to respond to PMSG, whereas growth of ovulatory follicles was stimulated in the other groups in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Gonadotropin and prolactin secretion following intraventricular administration of morphine in gilts.

The effects of central nervous system administration of morphine on secretion of luteinizing hormone (LH), follicle-stimulating hormone, and prolactin were investigated in ovariectomized gilts stereotaxically implanted with lateral ventricular cannulas. In Experiment 1, mean serum LH and follicle-stimulating hormone concentrations and serum LH pulse frequency were unaffected by artificial cerebrospinal fluid administration (P greater than 0.1), but decreased (P less than 0.01) in 8 of 11 gilts when 500 micrograms of morphine were given 3 hr later. Serum LH pulse amplitude was unaffected (P greater than 0.1) by cerebrospinal fluid or morphine injection. In Experiment 2, luteinizing hormone concentrations decreased (P less than 0.0001) and prolactin concentrations increased (P less than 0.0001), but follicle-stimulating hormone concentrations did not change (P greater than 0.1) after 500 micrograms of morphine. Gonadotropin responses to 10 micrograms of gonadotropin-releasing hormone, given 2 hr after intraventricular injection, were similar (P greater than 0.1) for morphine- and cerebrospinal fluid-treated gilts. These results indicate that morphine inhibits LH secretion at the level of the central nervous system, and are consistent with the concept that endogenous opioid peptides participate in the regulation of gonadotropin and prolactin release in pigs.

Absence of brain opioid peptide modulation of luteinizing hormone secretion in the prepubertal gilt.

Three experiments were conducted to evaluate the role of endogenous opioid peptides (EOP) in modulating luteinizing hormone (LH) secretion in the prepubertal gilt. In Experiment I, 8 prepubertal (P) gilts, 160-170 days of age (puberty = 197 +/- 10 days), received either 1 (n = 2), 3 (n = 3), or 6 (n = 3) mg/kg BW of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected by jugular vein cannula every 15 min for 2 h before and 2 h after NAL. All doses of NAL failed to alter serum LH concentrations. In Experiment II, 21 P gilts 160-170 days of age and 21 mature (M) gilts were ovariectomized (OVX). At the time of OVX, gilts were classified as prepubertal if their ovaries were devoid of corpora albicantia and corpora lutea. Three weeks after OVX, P and M gilts were injected twice daily for 10 days with either 0.85 mg/kg BW of progesterone (P4) or oil vehicle (V), resulting in the following groups: PP4 (n = 11), PV (n = 10), MP4 (n = 11), and MV (n = 10). All gilts received 1 mg/kg BW of NAL on the last day of treatment. Blood samples were collected via a jugular cannula every 15 min for 4 h before and 2 h after NAL treatment. NAL treatment resulted in an increase (p less than 0.05) in serum LH concentrations only in the MP4 gilts. In Experiment III, 15 OVX gilts 280 days of age were used. Ten of the 15 gilts were OVX prior to puberty at 160 days of age and were classified as chronologically mature (CM) at the time of treatment. The remaining 5 gilts were OVX after puberty, and were classified as sexually mature (SM) at the time of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Luteinizing hormone receptor number and affinity in corpora lutea from prepuberal gilts induced to ovulate and spontaneous corpora lutea of mature gilts.

This study was designed to determine if luteal cell receptors for luteinizing hormone/human chorionic gonadotropin (LH/hCG) contribute to the previously demonstrated abnormal function of induced corpora lutea (CL) in gilts. Twenty-five prepuberal (P) gilts, induced to ovulate with 1,500 IU pregnant mare serum gonadotropin followed 72 h later with 500 IU hCG (d 0 = day of hCG), and 22 mature (M) gilts that had displayed two or more estrous cycles were ovariectomized (OVX) on d 10, 14, 18, 22 or 26 after the onset of estrus. All gilts except those OVX on d 10 were hysterectomized between d 6 and 9 to ensure luteal maintenance. The CL were stored at -196 degrees C until determination of LH/hCG receptor number and dissociation constant (KD) by saturation analysis. Receptor number was greater for M than for P gilts on d 14 (P less than .07) and d 18 (P less than .01). The KD was greater in M than in P gilts on d 14 (P less than .01) and d 18 (P less than .0001). The LH/hCG receptor number and KD of P gilts remained the same throughout the days studied. The LH/hCG receptor number (fmol/mg protein) of M gilts was elevated on d 10, 14, and 18 (50.8, 50.4 and 51.4, respectively) and decreased on d 22 (26.5) and d 26 (25.4) to values similar to those of P gilts. In M gilts, KD increased on d 14, remained high on d 18 and decreased on d 22. We suggest that abnormal function of induced CL in P gilts may be due to an elevated LH receptor number.