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Biomedical subjects

N Parvizi

Publications and source records attributed to N Parvizi.

At least 19 recordsLinked to original sources

Foetal and neonatal development of luteinising hormone and its regulatory systems in the pig.

This review is a short summary of the "state-of-the-art" regarding the ontogeny of LH and part of its control system in the pig. The maturity of pituitary gonadotropin cells and the vascular drainage between the hypothalamus and pituitary are probably the most important steps in the developmental process of gonadotropin (LH) secretion. In the pig, these are achieved at around day 80 of foetal age, when LH cell density is comparable to that observed in adults. The hypothalamus regulates foetal pituitary LH secretion via LHRH well ahead of parturition. However, the main prerequisite of ovarian activity (ovulation), the "GnRH pulse generator", is not ready to function in the foetus. Pulsatile LH release is inducible by treatment of the foetal pituitary with LHRH, but extrahypothalamic modulating systems are not fully functioning until after birth. Likewise, there is no gonadal steroid feedback control of pituitary LH secretion up to the second week of neonatal age.

Analgesics, Opioid↗

LH and IGF-1 release during oestrus and early luteal phase in lactating and non-lactating horse mares.

The aim of the present study was to determine effects of lactation on basal LH and IGF-1 concentrations and on the LH response to a GnRH-analogue at different stages of the oestrous cycle in mares. A total of 17 cyclic Haflinger mares were included in the study. Experiments were performed on lactating mares in first postpartum oestrus, the subsequent early luteal phase, and second postpartum oestrus. Non-lactating mares were used in oestrus and early luteal phase. Blood samples were taken for 1 h at 15 min intervals. Mares were then injected with the GnRH-analogue buserelin (GnRHa; 5 microg i.v.) and blood samples were drawn every 15 min for further 2 h. LH in all samples and basal IGF-1-concentrations were determined by RIA. In lactating mares, basal LH concentrations during the early luteal phase tended to be lower (p = 0.07) and the LH response to GnRHa, calculated as area under the curve, was significantly less pronounced compared to non-lactating mares (p < 0.01). As well in lactating mares, the basal LH concentration between first early luteal phase and second oestrus differed significantly (p < 0.05) and the net response to GnRHa was significantly lower between first oestrus as well as second oestrus and first early luteal phase (p < 0.05) but not between first and second oestrous postpartum. Within the group of non-lactating mares, the LH response to GnRHa was as well significantly lower during oestrus than during early luteal phase (p < 0.01). IGF-1 concentrations differed neither between groups nor stages of the cycle within groups. In conclusion, basal and GnRHa-stimulated LH release in lactating mares is lower than in non-lactating mares. This difference, however, occurs only in the early luteal phase. In lactating mares, concentrations of LH appear adequate to allow ovulation to occur.

Animals↗

Effects of lactation on metabolic and reproductive hormones in Lipizzaner mares.

In this study, growth hormone (GH), insulin-like growth factor 1 (IGF-1), leptin, luteinising hormone (LH) and prolactin were analyzed in mares from late pregnancy throughout lactation (group 1, n=46) and in non-lactating mares (group 2, n=11). Plasma GH concentrations in group 1 mares during gestation and lactation were lower than in mares of group 2 (P<0.05). Highest IGF-1 levels were found in lactating mares in the week of foaling. IGF-1 concentrations decreased continuously thereafter. Plasma leptin concentrations decreased after foaling and, for 4 weeks, were lower in lactating than in non-lactating mares (P<0.05). Reduced leptin concentrations may promote feed intake and allow lactating mares to avoid an energy deficit. In group 1 mares, prolactin concentrations reached a maximum in the week of foaling and decreased rapidly thereafter. Plasma LH concentrations in group 1 mares before foaling were lower than at corresponding times in group 2 (P<0.05). LH concentrations then increased and did no longer differ from group 2 until week 2 postpartum. This increase may contribute to the resumption of cyclic ovarian activity in postpartum mares. Subsequently, LH levels in lactating mares decreased again (P<0.05). Increased IGF-1 concentrations early postpartum might contribute to ovarian stimulation while reduced IGF-1 and GH concentrations later in lactation might cause reduced stimulation. The changes in somatotrophic hormones could thus explain, at least in part, a more pronounced stimulation of ovarian function early postpartum than during the following months of lactation.

Animals↗

Dopaminergic and opioidergic regulation of gonadotropin and prolactin release in stallions.

In the non-breeding season, LH release is reduced via dopaminergic systems in the ram. On the other hand, our previous studies demonstrated an opioidergic inhibition of LH release in stallions outside the breeding season. Thus, in the present study we investigated the dopaminergic regulation of LH and prolactin secretion in stallions, considering interactions between dopamine and opioids. To achieve this, stallions (n=8) were treated with the dopamine antagonist sulpiride (0.6 mg/kg), the opioid antagonist naloxone (0.5 mg/kg), sulpiride plus naloxone or saline in December, March and June. Two hours after the respective treatments, they received a GnRH agonist. Sulpiride induced a significant prolactin release which was most pronounced in December, indicating seasonal variations in the inhibition of prolactin secretion by dopaminergic systems. Prolactin concentrations were not changed by naloxone. Neither during nor outside the breeding season, a dopaminergic regulation of LH release could be demonstrated. In contrast, naloxone caused a significant (p < 0.05) LH release, confirming an opioidergic inhibition of LH release. In conclusion, opioidergic regulation of LH and dopaminergic inhibition of prolactin secretion undergo seasonal changes. Neither during nor outside the breeding season, dopaminergic effects on LH release exist in the stallion.

Animals↗

Growth hormone secretagogue (GHS) analogue, hexarelin stimulates GH from peripheral lymphocytes.

The role of growth hormone releasing hormone (GHRH) and growth hormone releasing peptide-6 (GHRP-6) analogue hexarelin was investigated in the regulation of GH production from lymphocytes. Porcine and bovine blood mononuclear cells were separated using density gradient centrifugation method by layering the whole blood or buffy coat cells on lymphodex. Cells were incubated for 3 or 5 days with or without phytohemagglutinin (PHA-M), GHRH, GHRP-6 analogue hexarelin, somatostatin or GHRH + hexarelin. Growth hormone was fractionated from supernatants by gel chromatography and further concentrated by lyophilization at - 20 degrees C. A nearly two fold increase in basal secretion of GH (porcine: 3.5 +/- 0.1 ng/ml, bovine: 3.2 +/- 0.2 ng/ml) was achieved by GHRH and hexarelin at concentrations of 0.1, 1.0, 10 and 100 nM in both porcine and bovine cells. Lymphocytic GH release was also stimulated in response to PHA-M (10 micro g/well). Neither a dose dependent nor a synergistic nor an additive effect was apparent on GH secretion from lymphocytes. GHRH stimulated lymphocytic GH secretion, whereas, somatostatin had no effect. This study reports for the first time that hexarelin stimulates the secretion of GH from peripheral lymphocytes.

Animals↗

Nitric oxide and the control of reproduction.

The free radical gas, nitric oxide is now known to be an important biological messenger in animals. Signal transmission by a gas that is produced by one cell, penetrates through membranes and regulates the function of another cell, represents new principles for signalling in biological systems. Nitric oxide is synthesised from L-arginine by enzyme nitric oxide synthase, which exists in multiple isoforms in a wide range of mammalian cells. Studies conducted in recent years point at a strong influence of NO in a wide range of reproductive functions. It is implicated in the control of gonadotrophin secretion at both hypothalamic and hypophyseal levels, LH surge mechanism, sexual behaviour, estradiol synthesis, follicle survival and ovulation. While considerable work lies ahead in unravelling the role of NO at the peripheral, cellular and molecular level in the domestic animal reproduction, findings presented in this review provide a general overview of growing appreciation of NO as a vital molecule controlling hypothalamic-pituitary-gonadal (HPG) axis.

Animals↗

Neuroendocrine regulation of growth hormone and luteinizing hormone in fetal and neonatal pig.

Ontogeny of the production and the regulation of growth hormone and Luteinizing hormone is studied in a series of experiments utilizing male and female pigs at different fetal and neonatal stages. Growth hormone mRNA is detectable in both sexes as early as d. 50 p.c. The mRNA levels increase to reach the maximum levels at d. 95-110 p.c. Plasma levels of GH follow the developmental patterns of GH mRNA. A sex difference is evident around d. 80-90 p.c. with males having higher GH levels than females. The stimulatory but not the inhibitory mechanisms of GH secretion are fully functioning in the pig fetus. LHbeta mRNA is detectable earlier in females (d. 50 p.c.) than in males (d. 65 p.c.). Plasma concentrations of LH increase with fetal age in female fetuses, but in male fetuses there is no distinct developmental pattern evident. Basal LH secretion achieves maximum levels in both sexes after birth. Opioids do modulate fetal LH secretion, however, the mode of their action is age-dependent.

Animals↗

Pregnancy stimulates secretion of adrenocorticotropin and nitric oxide from peripheral bovine lymphocytes.

The cross-talk between the endocrine and the immune systems mediated by a wide array of hormones, cytokines, and neuromodulators is heightened during disease, stress, and presumably, during pregnancy. Adrenocorticotropin (ACTH) and nitric oxide (NO) are two immunomodulators that are also produced from lymphocytes and contribute to the immunomodulation. Thus, we investigated whether the heightened bidirectional communication between the immune and the endocrine systems observed during pregnancy is reflected in production of ACTH and NO from peripheral bovine lymphocytes and if any temporal correlation exists between them. Adrenocorticotropin was analyzed using a sandwich immunoradiometric assay, and nitrite and nitrate (a measure of NO) were estimated in supernatants of cultured peripheral blood lymphocytes (PBLs) using a colorimetric assay based on the Griess reaction. A significantly high secretion of ACTH and NO was noticed from PBLs in all stages of pregnancy compared to that in cyclic and cystic cows. Increased secretory capacity was noticed as early as 7 days after conception, which reached as much as 600% that of nonpregnant animals between Days 90-120 of gestation. Adrenocorticotropin and NO decline 1 mo before the expected time of parturition. Unlike those from cyclic animals, PBLs from pregnant cows were refractory to stimulation by PHA-M (Phytohemagglutinin) and corticotropin-releasing hormone. A strong correlation was observed between ACTH and NO secretion from PBLs in pregnant, in cyclic, and in cystic cows. To our knowledge, this is the first evidence elucidating the induction of ACTH and NO from PBLs during pregnancy, and it implies a new role for ACTH and NO secreted from PBLs in recognition and, probably, maintenance of pregnancy.

Adrenocorticotropic Hormone↗

Effects of morphine and naloxone on fetal heart rate and movement in the pig.

To test the hypothesis that an increasing opioid tonus is involved in decreases in fetal heart rate (FHR) and movement (FM) during late gestation, we studied the effects of intravenous bolus injections of morphine (1 mg) and naloxone (1 mg) on FHR and FM in the fetal pig. Twenty-one fetuses (1 per sow) were catheterized at 90-104 days of gestation (median 100 days). Recordings of FHR (electrocardiograph or Doppler-derived signals) and FM (ultrasonography) were made from 15 min before to 45 min after treatment. Morphine administration significantly decreased FHR, but it increased FHR variation and forelimb movements (LM). LM were clustered, and this stereotyped behavior has never before been observed in any mammalian fetus. Naloxone administration increased gross body movements and FHR without significant changes in FHR variation. It is concluded that FHR and motility are under opioidergic control in the pig fetus. Both morphine and naloxone induce hypermotility, suggesting that naloxone does not act as a pure opioid antagonist in the fetal pig.

Analgesics, Opioid↗

15-ketodihydro-PGF2 alpha, progesterone and cortisol profiles in heifers after induction of parturition by injection of dexamethasone.

In order to study rapid changes in 15-ketodihydro-PGF2 alpha, cortisol and progesterone in the period preceding parturition in cattle, pre-term parturition was induced in 4 late pregnant heifers. Parturitions were induced by 2 intramuscular injections of 20 mg dexamethasone with a 24-h interval. The first injection was made on days 254, 258, 264 and 265 in gestation, respectively. Twenty-four h before the first injection an intravenous polyurethane cannula was inserted. Blood samples were collected at least every hour until 12 h after parturition and during the second stage of labour at least 6 times per hour. Plasma was analysed for 15-ketodihydro-PGF2 alpha and progesterone by radioimmunoassays, and for cortisol by an ELISA. The average time from injection to parturition was 7.7 (6.6-8.9) days (mean (range)). Two of the heifers had retained foetal membranes (RFM). At the start of the experiment the levels of PGF2 alpha metabolite were low (< 300 pmol/L) and increased slowly to levels between 1000 and 2000 pmol/L at one day before parturition. During the last day, however, the levels increased rapidly and the highest levels (> 10,000 pmol/L) were reached at the time of delivery. No pulsatile release was seen. Immediately after foetal expulsion the PG-metabolite levels decreased rapidly in all animals. In the 2 animals with RFM, however, this decline ceased within a few h. The PG-metabolite levels in these animals then started to increase and reached levels as high as during parturition. Luteolysis occurred between 1.6 and 0.4 days before parturition in all animals. The cortisol profile showed a distinct peak at the time of parturition in the RFM heifers. This peak was absent in the non-RFM heifers. This study shows that the PGF2 alpha release at prepartal luteolysis and parturition is not pulsatile in cattle and that cortisol profiles in heifers with retained foetal membranes might differ from the profiles in non-RFM heifers at the time of parturition.

Animals↗

Opioidergic inhibition of luteinising hormone and prolactin release changes during pregnancy in pony mares.

In equine species, luteinising hormone (LH) and prolactin (PRL) release are reduced throughout pregnancy but increase at foaling. The present experiments were designed to study a possible opioidergic regulation of LH and PRL release in pregnant Shetland mares (n=6). At various stages of pregnancy (days 26.4+/-0.6, 75.4+/-5.4, 171.8+/-2.4, 226.2+/-4.8, 282.7+/-3.4 and 319.8+/-2.1), mares were injected with the opioid antagonist naloxone (0.5 mg/kg body weight) and saline. The two treatments were always separated by 2 days, and mares served as their own controls. Two hours after being given naloxone and saline, mares were given the gonadotrophin-releasing hormone (GnRH) analogue buserelin (5 microg per animal). The naloxone experiment was repeated at 2 days after foaling. Blood for the determination of LH and PRL was withdrawn at 15 min intervals for 240 min, and naloxone or saline was injected after 60 min. Naloxone induced significant (P<0.05) LH release on days 172, 226 and 283 of pregnancy but not on days 26, 76 and 320 and 2 days after foaling. Buserelin caused a significant (P<0.05) increase in plasma LH concentrations on days 172, 226, 282 and 320 of pregnancy. The experiments indicate that endogenous opioids are involved in the inhibition of LH release during the second half of pregnancy in equine species. The deactivation of opioid effects on LH release might be a prerequisite for the onset of ovarian activity postpartum. Plasma PRL concentrations increased significantly (P<0.05) after naloxone administration on days 226, 282 and 320 of pregnancy. The naloxone-induced PRL release was most pronounced towards term, indicating an increase in the naloxone-releasable pool and/or the absence of other PRL-release inhibitory mechanisms.

Animals↗

Transport stress modulates adrenocorticotropin secretion from peripheral bovine lymphocytes.

The influence of transport stress on the secretion of adrenocorticotropin (ACTH) from peripheral bovine lymphocytes was evaluated by exposing cows to short- (30 min) or long-term (14 h) transport. After transporting animals for 14 h they were given a mandatory rest for 24 h in two different situations, either by off-loading them and allowing them to rest in a stall or by keeping them in the truck. Blood samples were withdrawn before and after transport and after the rest period in long-term transported cows and before and after transport in cows transported for 30 min. Peripheral blood lymphocytes were separated and cultured for 72 h in serum-free medium. Adrenocorticotropin was measured using highly sensitive and specific immunoradiometric assay in culture supernates. We noticed no effect of short-term transport on ACTH secretion from lymphocytes. The ACTH concentration in animals transported for 14 h increased (P < or = 0.01) from 4.72 +/- 0.48 pg x mL(-1)/2 x 10(6) lymphocytes before the transport to 8.24 +/- 1.40 pg x mL(-1) directly after the transport. When animals were off-loaded and rested in a stall for 24 h, ACTH secretion from cultured lymphocytes returned to the basal value of 4.24 +/- 0.31 pg x mL(-1), whereas the animals rested in the truck had ACTH levels of 8.9 +/- 1.43 pg x mL(-1). Phytohemagglutinin, a plant lectin that stimulates lymphocytes, did not affect the lymphocytic ACTH secretion in this study. Heart rate and rectal temperature measured telemetrically increased in cows directly after 14 h of transport but decreased to pretransport values in cows rested for 24 h in cows rested in stalls and those rested inside the truck. This experiment is the first to show lymphocytic ACTH secretion in cows, and the results indicate that ACTH secretion from peripheral lymphocytes could be used as a reliable measurement in stress studies.

Adrenocorticotropic Hormone↗

Neuroendocrine regulation of gonadotropins in the male and the female.

For the past decade, neuroendocrinology, in general, and neuroendocrine regulation of reproduction, in particular, were strongly dominated by molecular genetics and molecular endocrinology. In very recent years, however, neuroendocrinology is taking back its place. Beyond doubt GnRH is the neuroendocrine signal for ovulation. But there are still many unexplored pathways within the 'black box' triggering and regulating this signal. Neuroendocrine control of reproduction starts very early in life, well before birth. Hypophyseal gonadotropin secretion is under hypothalamic control at around mid-gestation in the fetal sheep and the fetal pig. These two species could be considered as best-studied farm animals considering neuroendocrinology. This minireview thus will give in the first part a short survey of developmental processes of some of the neuroendocrine systems in the pig and sheep. In the second part, the opioidergic and catecholaminergic control of gonadotropins in adults will be briefly discussed. The last part will focus on the new less known pathways mediating effects on hormones which regulate the reproductive functions.

Aging↗

Myelin basic protein induces cell death of mature pig oligodendrocytes in vitro and produces demyelination in vivo.

Two methods prevail at present in producing demyelinated areas in the central nervous system. One uses the detergent-like effect of lysolecithin, the other is based on a cell killing effect of ethidium bromide plus x-irradiation. Unwanted side-effects are inherent in both methods. Based on the fact that myelin basic protein (MBP) kills adult pig oligodendrocytes but almost no astrocytes in vitro, we have used MBP for creating demyelinated areas in the centrum semiovale of the pig brain. These lesions are characterized by a loss of oligodendrocytes and myelin, a preservation of axons and astrocytes, and by the presence of macrophages. Thus, this type of lesion might present an alternative option for studying the fate of transplanted myelinating cells.

Animals↗

Plasma cortisol and ACTH concentrations in the warmblood horse in response to a standardized treadmill exercise test as physiological markers for evaluation of training status.

Reliable physiological markers for performance evaluation in sport horses are missing. To determine the diagnostic value of plasma ACTH and cortisol measurements in the warmblood horse, 10 initially 3-yr-old geldings of the Hannovarian breed were either exposed to a training schedule or served as controls. During experimental Phase 1, horses were group-housed, and half of the horses were trained for 20 wk on a high-speed treadmill. During Phase 2, groups were switched and one group was trained for 10 wk as during Phase 1, whereas the control group was confined to boxes. During Phase 3 horses were initially schooled for riding. Thereafter, all horses were regularly schooled for dressage and jumping, and half of the horses received an additional endurance training for 24 wk. During all phases horses were exposed at regular intervals to various standardized treadmill exercise tests. During and after the tests frequent blood samples were taken from an indwelling jugular catheter for determination of ACTH and cortisol. Treadmill exercise increased both hormones. Maximum ACTH concentrations were recorded at the end of exercise, and maximum cortisol levels were recorded 20 to 30 min later. Except for one test there were no differences in ACTH levels between trained horses and controls. There was no significant effect of training on the cortisol response (net increase) to treadmill exercise in any of the tests during Phase 1. During Phase 2 higher cortisol responses were recorded in controls than in trained horses (P < .05) after 10 wk of training (controls confined to boxes). During Phase 3 plasma cortisol responses were also higher in controls than in trained horses (P < .05 after 6, 18, and 24, P < or = .07 after 12 wk of training) when the inclination of the treadmill was 5%, but not at 3%. There was no overlap in net cortisol responses at 30 min between trained and untrained horses. An ACTH application after 24 wk of training resulted in higher cortisol responses in controls than in trained horses (P < or = .05), without any overlap between the groups at 30 min after ACTH. Plasma cortisol responses to either treadmill exercise or ACTH injection may be a reliable physiological marker for performance evaluation. Prerequisites are sufficient differences in training status and sufficient intensity of exercise test conditions.

Adrenocorticotropic Hormone↗

Concentrations of free steroids in the jugular and hepatic portal veins of pigs after ingestion of testosterone, estrogen, or progesterone or transplantation of ovaries to the intestine.

Estrogen, progesterone or testosterone were administered orally to ovariectomized gilts fitted with indwelling catheters. Blood samples were taken from the jugular and hepatic portal veins at intervals varying from a few minutes to daily over periods that varied from 1 d to several months. Concentrations of free steroids rose dramatically in the hepatic portal vein within a few min of feeding steroids and remained high for 3-8 hr before declining to base levels. Concentrations in the jugular vein sometimes rose very slightly for the same period. At 48 hr after administration the concentrations remained at baseline in the hepatic portal vein, but rose several-fold in the jugular and remained elevated for several days. Autotransplantation of the ovaries to the intestine resulted in very large ovaries consisting of many large, heavily luteinized cystic follicles. Concentrations of progesterone and estrogen in the hepatic portal vein were very high, but were low in the jugular vein. The gut wall allows for passage of some orally administered free steroids to the liver via the hepatic portal vein. The free steroids are essentially metabolized before they reach the jugular vein, but can be recirculated via the enterohepatic route.

Administration, Oral↗

Seasonal variation and opioidergic regulation of growth hormone release in cyclic, ovariectomized, and pregnant pony mares.

Modulation of reproductive functions is one of the multiple effects of growth hormone (GH). To investigate effects of reproductive functions on GH release in the horse, plasma GH concentrations in ovary-intact (n = 7) and ovariectomized (n = 8) mares during the anovulatory and breeding seasons and in pregnant mares (n = 6) at various stages of gestation were determined. To analyze an opioidergic regulation of GH release, repeated blood samples were taken over 3 h, and mares were injected with the opioid antagonist naloxone (0.5 mg/kg i.v.) or saline. GH was determined by RIA with an antiserum raised against porcine GH and equine GH as standard. In ovariectomized and ovary-intact, cyclic mares, GH concentrations were low and not different between the two groups in November and December. GH concentrations increased significantly (P < 0.05) in cyclic mares during May and June but were not affected by stage of the cycle and were low in ovariectomized mares. In pregnant mares, plasma GH concentrations remained high throughout pregnancy and did not decrease during winter but increased significantly (P < 0.05) postpartum. Naloxone induced a significant GH release in ovary-intact mares; this response was most pronounced (P < 0.05) during the breeding season. Naloxone did not affect GH in ovariectomized mares. During pregnancy, naloxone induced a significant release of GH around Day 280 (P < 0.05) but not at other times of pregnancy. In conclusion, GH release is influenced by season. The seasonal changes depend on ovarian factors, are absent in ovariectomized mares, and can be modulated by pregnancy. GH release is regulated at least in part by opioidergic pathways.

Animals↗

Compensation by pulsatile GnRH infusions for incompetence for oestradiol-induced LH surges in long-term ovariectomized gilts and castrated male pigs.

The aim of this study was to investigate incompetence for oestradiol-induced LH surges in long-term ovariectomized gilts and male pigs. Gilts (250 days old; n = 36), which had been ovariectomized 30 (OVX 30) or 100 days (OVX 100) before the start of treatment, were challenged i.m. with oestradiol benzoate and were either given no further treatment, fed methallibure to inhibit endogenous GnRH release or fed methallibure and given i.v. pulses of 100 or 200 ng GnRH agonist at 1 h intervals during the LH surge (48-96 h after oestradiol benzoate). The same treatments were applied to long-term orchidectomized male pigs (ORC, n = 23). In addition, one ORC group was not injected with oestradiol benzoate but was fed methallibure and given pulses of 200 ng GnRH agonist. Oestradiol benzoate alone induced an LH surge in the OVX 30 group only (5/6 gilts), methallibure suppressed (P < 0.05) oestradiol benzoate-induced LH secretion, while pulses of 100 ng GnRH agonist in animals fed methallibure produced LH surges in four of six OVX 30 and four of six OVX 100 gilts. The induced LH surges were similar to those produced by oestradiol benzoate alone in OVX 30 gilts. Pulses of 200 ng GnRH agonist produced LH surges in OVX 30 (6/6) and OVX 100 (6/6) gilts and increased the magnitude of the induced LH surge in OVX 100 gilts (P < 0.05 compared with 100 ng GnRH agonist or OVX 30 control). Pulses of 200 ng GnRH agonist also induced LH surge release in ORC male pigs (5/6), but were unable to increase LH concentrations in a surge-like manner in ORC animals that had not been given oestradiol benzoate, indicating that oestradiol increases pituitary responsiveness to GnRH. These results support the hypothesis that oestradiol must inhibit secretion of LH before an LH surge can occur. It is concluded that incompetence for oestradiol-induced LH surges in long-term ovarian secretion-deprived gilts and in male pigs is due to the failure of oestradiol to promote a sufficient increase in the release of GnRH.

Analysis of Variance↗