Hormonal profile and morphological changes in pig ovaries after intraovarian infusions of Escherichia coli endotoxin

The purpose of this study was to estimate morphological changes in the ovary and size of the production of steroid hormones during the luteal phase of the estrous cycle in pigs after intraovarian infusions of Escherichia coli endotoxin. Polish Large White gilts (n = 15) of similar age (7-8 months) and body weight (90-110 kg) with two controlled subsequent estrous cycles were used. The animals were randomly divided into two groups: control (n = 9, the 10th day of the estrous cycle,) and treated with Escherichia coli endotoxin (n = 6, the same day of the estrous cycle). The gilts were infused with Escherichia coli endotoxin at a dose of 1 mg three times a day during six consecutive days, from the 14th to the 19th day of the estrous cycle. Plasma concentrations of progesterone (P4), androstenedione (A4), testosterone (T), estrone (E1) and estradiol-17 beta (E2) were determined by radioimmunoassay method. Infusions of Escherichia coli endotoxin resulted in a significant (p < 0.001) decrease in the production of P4, A4, T, E1 and E2 in the luteal phase as compared with the levels found in the control animals. Plasma level of P4, A4 and T was decreased by 84.6%, 86.0% and 73.0%, respectively. Plasma concentrations of E1 and E2 in some cases exceeded 5 pg/ml, nevertheless in the majority of the samples they were under sensitivity of the method. Escherichia coli endotoxin infusions resulted in a considerable decrease in the size of the ovaries, and morphological changes characteristic for acute and chronic inflammation were observed.     

Anovulation and plasma hormone concentrations after administration of dexamethasone during the middle of the luteal phase in sows undergoing estrous cycles

The effect of glucocorticoids on early follicular growth in sows undergoing normal estrous cycles was evaluated by administration of dexamethasone during the middle of the luteal phase. Plasma specimens were obtained for measurement of luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and estradiol-17 beta concentrations. Fifteen sows were used. Control sows (n = 5) were given physiologic saline solution twice daily from day 9 to day 14 of the estrous cycle. Sows of the second group (n = 5) were given dexamethasone (30 micrograms/kg of body weight, IM) similarly, and those of the third group (n = 5) were given dexamethasone plus gonadotropin-releasing hormone (GnRH; 50 micrograms at 6-hour intervals, IV). Plasma specimens, obtained twice daily from day 8 through day 26, indicated that progesterone production and luteal regression were not inhibited by any of the 3 treatment regimens. Although preovulatory plasma estradiol concentration increased in control sows, such was not observed in the sows treated with dexamethasone or dexamethasone plus GnRH (P less than 0.01). Ovulation, with formation of corpora lutea, occurred in gilts given saline solution. Dexamethasone administration resulted in persistence of 19 to 41 follicles/ovary (2 to 4 mm in diameter), and dexamethasone-plus-GnRH treatment resulted in 6 to 18 follicles/ovary (5 to 6 mm in diameter). Plasma was obtained at 15-minute intervals for 12 hours to compare the effect of treatment on hormone concentrations on day 12 of the estrous cycle with the values on day 8.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Effect of human chorionic gonadotropin on preovulatory luteinizing hormone surge and ovarian hormone secretion in gilts

The influence of varying doses of human chorionic gonadotropin (hCG) on the preovulatory luteinizing hormone (LH) surge, estradiol-17 beta (E2) and progesterone (P4) was studied in synchronized gilts. Altrenogest (AT) was fed (15 mg X head-1 X d-1) to 24 cyclic gilts for 14 d. Pregnant mares serum gonadotropin (PMSG; 750 IU) was given im on the last day of AT feeding. The gilts were then assigned to one of four groups (n = 6): saline (I), 500 IU hCG (II), 1,000 IU hCG (III) and 1,500 IU hCG (IV). Human chorionic gonadotropin or saline was injected im 72 h after PMSG. No differences in ovulation rate or time from last feeding of AT to occurrence of estrus were observed. All gilts in Groups I and II expressed a preovulatory LH surge compared with only four of six and three of six in Groups III and IV, respectively. All groups treated with hCG showed a rapid drop (P less than .01) in plasma levels of E2 11, 17, 23 h after hCG injection when compared with the control group (35 h). The hCG-treated gilts exhibited elevated P4 concentrations 12 h earlier than the control group (3.1 +/- .5, 3.4 +/- .72, 3.1 +/- .10 ng/ml in groups II, III and IV at 60 h post-hCG vs .9 +/- .08 ng/ml in group I; P less than .05). These studies demonstrate that injections of ovulatory doses of hCG (500 to 1,500 IU) had three distinct effects on events concomitant with occurrence of estrus in gilts: decreased secretion of E2 immediately after hCG administration, failure to observe a preovulatory LH surge in some treated animals and earlier production of P4 by newly developed corpora lutea.     

Plasma gonadotropins and ovarian hormones during the estrous cycle in high compared to low ovulation rate gilts

Mature gilts classified by low (12 to 16 corpora lutea [CL], n = 6) or high (17 to 26 CL, n = 5) ovulation rate (OR) were compared for plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), progesterone, estradiol-17beta, and inhibin during an estrous cycle. Gilts were checked for estrus at 8-h intervals beginning on d 18. Blood samples were collected at 8-h intervals beginning on d 18 of the third estrous cycle and continued for one complete estrous cycle. Analysis for FSH and LH was performed on samples collected at 8-h intervals and for ovarian hormones on samples collected at 24-h intervals. The data were standardized to the peak of LH at fourth (d 0) and fifth estrus for the follicular phase and analyzed in discrete periods during the periovulatory (-1, 0, +1 d relative to LH peak), early-luteal (d 1 to 5), mid-luteal (d 6 to 10), late-luteal (11 to 15), periluteolytic (-1, 0, +1 d relative to progesterone decline), and follicular (5 d prior to fifth estrus) phases of the estrous cycle. The number of CL during the sampling estrous cycle was greater (P < 0.005) for the high vs low OR gilts (18.8 vs 14.3) and again (P < 0.001) in the cycle subsequent to hormone measurement (20.9 vs 14.7). For high-OR gilts, FSH was greater during the ovulatory period (P = 0.002), the mid- (P < 0.05) and late-luteal phases (P = 0.01), and tended to be elevated during the early-luteal (P = 0.06), but not the luteolytic or follicular periods. LH was greater in high-OR gilts during the ovulatory period (P < 0.005), but not at other periods during the cycle. In high-OR gilts, progesterone was greater in the mid, late, and ovulatory phases (P < 0.005), but not in the follicular, ovulatory, and early-luteal phases. Concentrations of estradiol-17beta were not different between OR groups during the cycle. Inhibin was greater for the high OR group (P < 0.005) during the early, mid, late, luteolytic, and follicular phases (P < 0.001). The duration of the follicular phase (from last baseline estrogen value to the LH peak) was 6.5 +/- 0.5 d and was not affected by OR group. These results indicate that elevated concentrations of both FSH and LH are associated with increased ovulation rate during the ovulatory phase, but that only elevated FSH during much of the luteal phase is associated with increased ovulation rate. Of the ovarian hormones, both inhibin and progesterone are highly related to greater ovulation rates. These findings could aid in understanding how ovulation rate is controlled in pigs.     

Ovarian response to pregnant mare serum gonadotropin and porcine pituitary extract in gilts actively immunized against gonadotropin releasing hormone

Two experiments were conducted to determine the effect of exogenous gonadotropins on follicular development in gilts actively immunized against gonadotropin releasing hormone (GnRH). Four gilts, which had become acyclic after immunization against GnRH, and four control gilts were given 1,000 IU pregnant mare serum gonadotropin (PMSG), while four additional control gilts were given saline. Control animals were prepuberal crossbred gilts averaging 100 kg body weight. Control gilts given saline had ovaries containing antral follicles (4 to 6 mm in diameter). Control gilts given PMSG exhibited estrus and their ovaries contained corpora hemorrhagica and corpora lutea. PMSG failed to stimulate follicular growth in gilts immunized against GnRH, and ovaries contained regressed corpora albicantia and small antral follicles (less than 1 mm in diameter). Concentrations of luteinizing hormone (LH) and estradiol-17 beta (E2) were non-detectable in gilts immunized against GnRH and given PMSG. In the second experiment, five gilts actively immunized against GnRH were given increasing doses of PMSG every third day until unilateral ovariectomy on d 50. PMSG failed to stimulate follicular growth, and concentrations of follicle stimulating hormone (FSH), E2 and LH were not detectable. Six weeks later, gilts were given a booster immunization and then were given 112 micrograms LH and 15 micrograms FSH intravenously every 6 h for 9 d. The remaining ovary was removed on d 10. Although LH and FSH concentrations were elevated, administration of gonadotropins did not stimulate follicular growth or increase E2 concentrations. These results indicate that neither PMSG or exogenous LH and FSH can induce E2 synthesis or sustain follicular development in gilts actively immunized against GnRH.     

Concentrations of Tissue-Type Plasminogen Activator and Relaxin in Normal and Induced-Cystic Follicles of Gilts

Manipulation of one ovary in prepubertal gilts treated with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) results in cysts on the manipulated ovary and corpora lutea (CL) on the non-manipulated (control) ovary. Because tissue-type plasminogen activator (tPA) might play a role in follicular rupture and because relaxin might increase tPA production, concentrations of tPA and relaxin in manipulated and control follicles were measured at different stages of development. Prepubertal gilts were treated with 1000 IU PMSG followed by 750 IU hCG at 72 hr later. Follicles on one ovary in each gilt were manipulated at laparotomy 48 hr after PMSG administration. Gilts were ovariectomized at 72, 90, 108, 114, 144, and 216 hr after PMSG. Concentrations of tPA and relaxin were determined for follicular fluid from follicles dissected free of ovarian stroma and snap frozen in liquid nitrogen and media from follicles cultured for 48 hr. Relaxin did not differ between treatment groups (manipulated and control) at any time (P > 0.05); whereas, tPA was greater in control follicles at 114 hr after PMSG than in manipulated follicles (P < 0.01). The effect of pyrilamine, a histamine-1 receptor antagonist, on tPA concentrations was determined in manipulated and control follicles collected at 3, 12, 24, 42, and 66 hr after manipulation. Concentrations of tPA were similar in control and manipulated follicles for gilts treated with pyrilamine, but again control follicles had greater (P < 0.05) tPA concentrations at 114 hr after PMSG. Thus, tPA seems to be involved in ovulation, and blockage of ovulation and subsequent cyst formation results from inadequate tPA activity in manipulated follicles.     

Observations on the influence of exogenous gonadotrophins and cloprostenol on ovulation in gilts

We studied the effects of gonadotrophins and prostaglandin (PG) F_2α on ovulation in gilts. Twenty-eight gilts were induced to ovulate using 750 IU pregnant mares serum gonadotrophin (PMSG) and 500 IU human chorionic gonadotrophin (hCG), administered 72 h apart. At 34 and 36 h after hCG, gilts received injections of either 500 μg or 175 μg PGF_2α (cloprostenol), or had no injections. Laparotomies were performed at 36 h (cloprostenol gilts) or 38 h (controls) after hCG injection. The ovaries were examined and the proportion of preovulatory follicles that had ovulated (ovulation percent) was determined at 30 min intervals for up to 6 h. The number of gilts in which ovulation was initiated and the ovulation percent increased (p<0.001) with time, but was not affected by treatment. Many medium sized follicles (≤6 mm) were also observed to ovulate, or to exhibit progressive luteinization without overt ovulation, during the surgical period. A discrepancy between numbers of preovulatory follicles and corpora lutea suggests that luteal counts may not be an accurate assessment of ovulation rate following gonadotrophic stimulation.     

The influence of male pheromones on the contractile reactivity of the isolated superficial veins of the nose and face during the estrous cycle in gilts

This study was designed to determine whether steroid sex pheromones of the boar may affect the contractile activity of the superficial venous vessels of the nose and face in gilts, and in this way contribute to recently discovered humoral transfer of pheromones to the brain and hypophysis. The dependence between the reactivity of nasal and facial veins to male pheromones and the phase of the estrous cycle in gilts was also studied. The gilts were used in the luteal phase of the cycle and in the follicular phase of the cycle. The dorsal nasal, frontal and facial veins were isolated on an appropriate day of the estrous cycle. The isolated rings of veins were treated with androstenone (5alpha-androst-16-en-3-one), androstenol (5alpha-androst-16-en-3-ol) and testosterone (17beta-hydroxy-4-androsten-3-one) in concentrations of 1 or 10 microM. Changes in the contractile activity of the isolated vein segments were measured using isometric transducer and recorded on HSE-ACAD software for Windows. Androstenone--main signaling boar pheromone--induced much stronger reactions of the vessels than androstenol. Androstenone caused significant relaxation of the dorsal nasal and frontal veins, and significant increased tension of the facial vein in the follicular phase of the estrous cycle. The results obtained suggest a direct effect of male pheromones on the contractile reactivity of the superficial veins of the nose and face in the female, and in this way contribute to a humoral pathway for transfer of pheromones to the brain and hypophysis. Moreover, the present study revealed changes in the reactivity during the estrous cycle of the veins, transporting blood from the region of the nasal cavity, to male pheromones participating in the regulation of female reproductive processes.     

Secretion of luteinizing hormone into pituitary venous effluent of the follicular and luteal phase mare: novel acceleration of episodic release during constant infusion of gonadotropin-releasing hormone

We tested the hypothesis that continuous infusion of native GnRH into mares during the estrous cycle, at a dose of 100 μg/h, would elevate circulating concentrations of LH without disrupting the endogenous, episodic pattern of LH release. Ten cyclic mares were assigned to one of two groups (n = 5/group): (1) Control (saline) and (2) GnRH in saline (100 μg/h). On experimental day 0 (3 to 6 d after ovulation), osmotic pumps containing saline or GnRH were placed subcutaneously and connected to a jugular infusion catheter. Blood samples were collected from jugular catheters daily and at 5-min intervals from catheters placed in the intercavernous sinus (ICS) for 8 h on experimental day 4 (luteal phase; 7 to 10 d after ovulation), followed by an additional 6-h intensive sampling period 36 h after PGF(2α)-induced luteal regression (experimental day 6; follicular phase). Treatment with GnRH increased (P < 0.001) concentrations of LH by 3- to 4-fold in the peripheral circulation and 4- to 5-fold in the ICS. Continuous GnRH treatment accelerated (P < 0.01) the frequency of LH release and decreased the interepisodic interval during both luteal and follicular phases. Treatment with GnRH during the luteal phase eliminated the low-frequency, long-duration pattern of episodic LH release and converted it to a high-frequency, short-duration pattern reminiscent of the follicular phase. These observations appear to be unique to the horse. Further studies that exploit this experimental model are likely to reveal novel mechanisms regulating the control of gonadotrope function in this species.     

The effect of fixed-time artificial insemination protocol initiated at different stages of the estrous cycle on follicle development and ovulation in gilts

Hormonal products have been developed for fixed-time artificial insemination (FTAI) to improve the efficiency of swine production. Here, we evaluated the effect of an FTAI protocol initiated during different phases of the estrous cycle on follicle development and ovulation in gilts. A total of 36 gilts were equally divided into three groups designated as the luteal (L), follicular (F), and post-ovulation (O) groups and fed with 20 mg of altrenogest for 18 days, followed by intramuscular injection of 1000 IU PMSG at 42 h after withdrawal of altrenogest, and 100 μg of GnRH after an 80-h interval. The L group had the highest number of follicles 4–6 mm in diameter, as well as corpora hemorrhagica. The mRNA expression of caspase-9 in the L group were significantly lower than those in the O and F groups (P < 0.05), while CYP11A1 and VEGF mRNA expression levels were significantly higher (P < 0.05). Moreover, FSHR mRNA levels were significantly higher in the O group than in the L, F, and control groups (P < 0.05). LHCGR and CYP19A1 mRNA levels were the highest in the F group (P < 0.05). Thus, the changes in the expression of genes associated with follicular development, maturation, and ovulation identified in this study indicated that initiation of the FTAI protocol during the luteal phase induced a better environment for follicle development and ovulation in gilts.     

Estrous cycle-dependent differences in responsiveness to prostaglandins and contractile agents in sheep (Ovis aries) cervical smooth muscle

We investigated the influence of the phase of the estrous cycle on mechanical responses elicited in sheep cervix by potassium chloride (KCl), acetylcholine chloride (ACh), prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E1 (PGE1). The cervix of adult ewes (n = 48) were classified according to the presence or absence of corpora lutea (luteal or follicular phase, respectively). Muscle strips of the circular and longitudinal layers were prepared in an organ bath and coupled to an isometric force transducer. Concentration-response curves were obtained noncumulatively. KCl and ACh produced concentration-dependent contractions in all preparations in both phases of the estrous cycle. However, maximum effect, EC50 and slope values of KCl and ACh were not significantly different between muscle layers, as well as between the phases of the estrous cycle. The prostanoid, PGF2 alpha, produced a significant reduction in the amplitude of spontaneous contractions for all preparations. The depressant effect of PGF2 alpha on spontaneous contractions of circular smooth muscle was significantly greater during the follicular than the luteal phase, whilst the depressant effect of PGF2 alpha on the longitudinal layer did not differ between phases of the estrous cycle. PGE1 significantly reduced the amplitude of spontaneous contractions on circular but not on longitudinal preparations. In conclusion, we have characterized with in vitro preparations of circular and longitudinal muscle layers of ewes during the follicular and luteal phases of the estrous cycle, the parameters of the K- and ACh-induced contractions on cervix and the efficacy of PGF2 alpha and PGE1 on inhibition spontaneous contractile activity.     

Leptin infusion during the early luteal phase in ewes does not affect progesterone production

Infusion of leptin during the ovine follicular phase has been shown to increase progesterone secretion during the subsequent luteal phase. In this study, we have assessed the effects of infusing leptin during the early luteal phase. Infusion of leptin (2.5 microg/h) into the ovarian artery of ewes with ovarian autotransplants (n=5) on day 3 of the luteal phase for 12h did not affect progesterone estradiol or LH concentrations compared to control ewes (n=5). These results suggest no direct effect of leptin on ovarian function at this stage of the estrous cycle.     

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.     

Food deprivation stimulates the luteolytic capacity in the gilt

The aims of this study were to study the effects of fasting on progesterone (P4) production in the pig and to verify whether fasting influences luteal expression of PGF(2alpha) receptor (FPr) and prostaglandin secretion. Superovulated prepubertal gilts were used; half of them were fasted for 72h starting on day 2 (F2) or 9 (F9) of the induced estrous cycle, respectively, while two groups (C2 and C9) served as respective controls. Plasma P4 and PGFM concentrations were determined by RIA while FPr mRNA expression in CLs collected at the end of fasting period was measured by real-time PCR. In experiment 1, plasma P4 concentrations in fasted gilts were significantly (P<0.01) higher than in controls starting from day 3 (F2; n=6) and 10 (F9; n=6). FPr mRNA expression was similar in F2 and C2 (n=6) CLs while it was significantly (P<0.05) higher in F9 than in C9 (n=6) CLs. In experiment 2, cloprostenol administered on day 12 significantly (P<0.05) increased FPr mRNA expression in CLs from both F9 (n=6) and C9 (n=6) gilts. At the time of cloprostenol injection PGFM levels were significantly higher (P<0.05) in the fasted group and cloprostenol-induced luteolysis in fasted but not in normally fed gilts. Results from this study indicate that fasting in prepubertal gilts induced to ovulate stimulates luteal P4 and PGFM production as well as FPr mRNA expression, thus increasing luteolytic susceptibility.     

Ovarian response of the hypophysial stalk-transected pig to pregnant mare serum gonadotropin

Hypophysial stalk transection (HST) or sham operation (S-HST) was performed on 14 prepuberal gilts, 169 ± 3 days of age and 72.8 ± 3.4 kg body weight (day of surgery = Day 0). Gilts received 1,000 IU of pregnant mare's serum gonadotropin (PMSG) or saline vehicle (V) intramuscularly (im) on Day 2 resulting in the following groups: S-HST + V (n=3), S-HST + PMSG (n=4), HST + V (n=3) and HST + PMSG (n=4). Ovarian morphology and weights were recorded after ovariectomy on Day 6. Gilts were weighed on Day 59 ± 3. Sequential blood samples were collected via jugular vein cannula from 6 S-HST and 6 HST gilts on Day 60 ± 3, and all gilts were necropsied on Day 86 ± 7. Body weight gain and whole pituitary gland weight were greater (P<0.05) for S-HST than HST gilts. Mean serum LH concentration, basal serum LH concentration, frequency of LH peaks and LH peak amplitude were greater (P<0.005) for S-HST than HST gilts. Serum PRL and GH, were similar for both groups. Total ovarian and follicular fluid weights were greater (P<0.05) in S-HST gilts given PMSG than those of the other three groups which did not differ. Therefore, PMSG stimulated follicular growth in S-HST gilts, but failed to stimulate follicular growth in HST gilts. We suggest that a critical basal serum LH and/or FSH concentration must be maintained to support and promote follicular growth and a pulsatile delivery of GnRH to the anterior pituitary gland by an intact brain-pituitary unit may be required to provide this basal serum gonadotropin concentration.     

Opioid inhibition stimulates luteinizing hormone and prolactin secretion in the gilt

Ten gilts on day 6·11 of the estrous cycle (onset of estrus = day 0) were given 115 mg of naloxone (NAL), an opioid antagonist, in saline i.v. (n = 5) or saline Lv. (n = 5). Jugular blood was collected at 15 min intervals for 2 hr before and 4 hr after treatment. Serum LH concentrations were 0.4 ± 0.1 ng/ml before NAL treatment, increased (P<.01) to 4.3 ± 0.7 ng/ml at 15 min following NAL treatment and returned to control concentrations by 75 minutes. Serum PRL concentrations were 5.0 ± 0.1 ng/ml before NAL treatment, increased (P<.05) to 14.8 ± 2.9 ng/ml at 30 min following NAL treatment and returned to control concentrations by 120 minutes. Serum LH and PRL concentrations were 0.5 ± 0.1 ng/ml and 5.2 ± 0.4 ng/ml, respectively, at 15 min following saline treatment and remained unchanged throughout the blood sampling period. Four of the 5 NAL treated gilts responded with an increase in both serum LH and PRL concentrations. The mean of serum progesterone concentrations, quantitated in samples taken every 2 hr, were similar for controls (22.7 ± 1.8 ng/ml) and NAL (26.5 ± 1.4 ng/ml) treated gilts. The gilt which failed to respond to NAL had nondetectable concentrations of serum progesterone and was excluded from analysis. These data indicate that the opioids modulate LH and PRL secretion during the luteal phase of the estrous cycle.     

Nutritionally induced body weight loss and ovarian quiescence in Shiba goats

Four female Shiba goats were used to determine the influence of body weight loss by dietary restriction on estrous cyclicity. The dietary restriction was started on the day following ovulation. The goats were fed hay cube and straw at an amount of 30% of energy requirement based on weekly body weight measurement. The ovaries were monitored daily by transrectal ultrasonography and blood samples were collected daily by jugular venipuncture for ovarian steroids analysis. After the start of food restriction, all animals lost body weight and entered ovarian quiescence. Intervals to the onset of ovarian quiescence tended to depend on the body weight of each animal at the start of food restriction. The mean concentration of progesterone during the mid-luteal phase (from 7 to 13 days after ovulation) in the last estrous cycle before ovarian quiescence was significantly lower than that in normal estrous cycle of the control period (19.7 +/- 2.8 vs 12.3 +/- 2.2 ng/ml, P<0.05), whereas there was no significant difference in the length of the luteal phase, determined as the period when corpora lutea existed and concentrations of progesterone were equal to or greater than 1 ng/ml (15.8 +/- 1.5 vs 15.0 +/- 2.8 days, P>0.1). A rise of estradiol concentration and follicular growth in the follicular phase following a decline of progesterone level after luteal regression tended to be suppressed at the onset of ovarian quiescence. It seems that the present results are consistent with previous findings that nutritionally induced body weight loss influences the secretion of ovarian steroids and eventually induces ovarian quiescence.     

Synchronized Induction of Pubertal Estrus in Gilts with Gonadotropins and Prostaglandin F2α Analogs: Clinical Observation.

Contents Clinical field observations on more than 7 500 pubertal gilts from four breeds and several locations, but under similar management, are reported. Standard procedures with pubertal gilts (grouping, special diets, boar exposure) did not bring sufficient numbers of gilts into heat within the first 6 days after grouping for efficient use of artificial insemination. Adding treatment with PMSG/hCG on day one of grouping, doubled the percentage of gilts in heat by day 6, from 25–30% to 57–60%. Treatment on day 1 with the PGF analogs alfaprostol or Enzaprost, followed by PMSG/hCG on day 5, increased the percentage of gilts in heat from 10–15% during the first 5 days to 75–80% between days 6 and 10. Hormonal treatments enlarged litter size by 0.5–0.7 piglets, respectively.     

Changes in Ovarian Follistatin Levels During the Oestrous Cycle in Sheep may Serve as an Intraovarian Regulator

The expression and concentration of follistatin and activin change during oestrous cycle suggesting their involvement in the regulation of follicular development. The aim of this study was to determine the level, source and potential role of follistatin in the sheep ovary. Follistatin in ovarian venous blood, measured by radioimmunoassay, remained at its low level from follicular phase (day ?1 and 0) to mid‐luteal phase (days 11–13) phase but were significantly elevated during the late luteal phase (days 14 and 15) when corpora lutea underwent regression. Western blot analyses of follicular fluid at day 15 of the cycle showed two strong bands at 42 and 45 kDa and weakly stained bands at 39 and 31 kDa. At day 0, these bands became weaker and the 39 kDa band became undetectable. However, there were no differences in follistatin concentrations between ovaries with and without functional corpus luteum (CL) during the whole luteal phase. In addition, although the ovaries of Booroola ewes normally contain more corpora lutea than those of normal merino ewes, follistatin concentrations in both jugular and ovarian venous blood were similar in Booroola and normal merino ewes. It is concluded that the secretion of follistatin from the ovary is not related to the formation of CL or high ovulation rate of Booroola ewes. The elevation in follistatin concentration in follicular fluid and ovarian blood during late luteal phase may indicate a dual role of follistatin in the luteolysis of existing CL and development of new follicle cohort.