Non-steroidal factors in bovine follicular fluid inhibit or facilitate the action of pulsatile administration of GnRH on LH release in the female rat.

Using steroid-free bovine follicular fluid (bFF), we studied the action of gonadotrophin surge-inhibiting factor/attenuating factor (GnSIF/AF) on GnRH-induced self-priming in phenobarbital-blocked female rats. For the experiments we used intact rats, short-term (4 h) ovariectomized (OVX) rats and long-term (14 days) OVX rats. In the latter case the rats were injected with 17beta-oestradiol benzoate (OB, 40 micrograms) or vehicle only, 2 or 48 h before the experiment.

Immunoneutralization of follicle stimulating hormone does not affect gonadotrophin surge-inhibiting factor/attenuating factor bioactivity during the rat ovarian cycle.

The physiological role of follicle stimulating hormone (FSH) in the regulation of the release of the putative ovarian factor gonadotrophin surge-inhibiting or -attenuating factor (GnSIF/AF) was investigated. Blood FSH concentrations were immunoneutralized in female rats during different days of the ovarian cycle. FSH antiserum was injected in different protocols to neutralize the FSH surge(s) and/or basal FSH concentrations.

From basal luteinizing hormone (LH) concentrations to the pre-ovulatory LH surge: titration of the physiological effect of gonadotrophin surge-inhibiting/attenuating factor.

Pulsatile luteinizing hormone (LH) release is thought to be controlled by the functional antagonism between gonadotrophin-releasing hormone (GnRH) and the putative ovarian factor gonadotrophin surge-inhibiting/attenuating factor (GnSIF/AF). Our experiments were designed to titrate the input of endogenous basal and follicle stimulating hormone (FSH)-stimulated GnSIF/AF in this system. The effects were studied of five consecutive pulses of GnRH administration (10-250 pmol/pulse/kg rat), 1 h apart, on the self-priming effect in pro-oestrus phenobarbital-blocked rats injected with FSH or saline.

[Dehorning of goats and kids].

The local anaesthesia used during the dehorning of goats is described. The authors recommend general anaesthesia for the disbudding (dehorning) of kids. In addition to the dehorning of goats and kids, this article also describes the use of the combination of xylazine, ketamine, and atropine, and the preparation of this 'goat anaesthetic'.

On the dynamics between gonadotrophin surge-inhibiting factor and gonadotrophin releasing hormone (GnRH): role of self-priming and desensitization in the luteinizing hormone response to GnRH after follicle stimulating hormone treatment.

The effects were studied of follicle stimulating hormone (FSH)-induced production of gonadotrophin surge-inhibiting factor (GnSIF) on three phases of the pituitary responsiveness to gonadotrophin releasing hormone (GnRH): the unprimed, primed and desensitized phases. Rats were injected with FSH on two occasions during the oestrous cycle. Spontaneous luteinizing hormone (LH) surges were measured as well as GnRH-induced LH surges on the day of pro-oestrus during infusions with 100-4000 pmol GnRH/rat/10 h, in phenobarbital blocked rats.

Induction of the gonadotrophin surge-inhibiting factor by FSH and its elimination: a sex difference in the efficacy of the priming effect of gonadotrophin-releasing hormone on the rat pituitary gland.

This study was designed to explore the efficacy of gonadotrophin-releasing hormone (GnRH) to antagonize the effect of gonadotrophin surge-inhibiting factor (GnSIF) on the timing of the induction by GnRH of the maximal self-priming effect on pituitary LH responsiveness. The GnSIF levels were increased by FSH treatment and reduced after gonadectomy. Female rats were injected s.

Effects of the opioid antagonist naltrexone-estrone azine on the luteinizing hormone-releasing hormone induced release of luteinizing hormone from the pituitary glands of ovariectomized rats.

The effects were studied of in vivo administration of the new opioid antagonist-estrogen hybrid, naltrexone-estrone azine (EH-NX), on subsequent luteinizing hormone-releasing hormone (LHRH)-stimulated luteinizing hormone (LH) release by the pituitary gland in vitro. It is well known that administration of estrogen exerts negative and positive effects on the pituitary LH response to LHRH, respectively after short-term and long-term treatment. Rats were injected subcutaneously with either 17 beta-estradiol-3-benzoate (EB), EH-NX or oil on days 18 and 19 (long-term treatment), and on day 21 (short-term treatment) following ovariectomy.

Estrogenic effects of the new opioid antagonist naltrexone-estrone azine on pituitary luteinizing hormone secretion in ovariectomized rats.

The effect of the new opioid antagonist naltrexone-estrone azine (EH-NX) on pituitary luteinizing hormone (LH) secretion in the ovariectomized rat was studied. EH-NX is a hybrid between the steroid component estrone and the opioid antagonist naltrexone (NX). It is a potent and long-acting opioid antagonist in vitro and in vivo, but its effect upon in vivo LH secretion has not been tested before.

The self-priming action of LHRH is under negative FSH control through a factor released by the ovary: observations in female rats in vivo.

Female rats were treated with Metrodin (highly purified urinary FSH from menopausal women) or saline during the oestrous cycle. On the day of pro-oestrus they were anaesthesized with phenobarbital and received four repetitive LHRH injections 1 h apart. This treatment with FSH suppressed the unprimed LH response to the first LHRH injection.

Autonomous FSH synthesis in vitro in anterior pituitary glands and grafts from female rats.

When pituitary glands from intact female, but not from ovariectomized rats, are incubated for 8 h in medium TC199 without further additives, FSH is synthesized. This LHRH-independent (or autonomous) FSH synthesis is prevented when bovine follicular fluid (bFF) is added to the incubation medium. Results from preliminary experiments, however, indicate no clear autonomous FSH synthesis after long-term absence of LHRH.

Testicular weight, tubular diameter and number of Sertoli cells in rats are decreased after early prepubertal administration of an LHRH-antagonist; the quality of spermatozoa is not impaired.

To suppress gonadotropin secretion during the sensitive period in development of the testes, immature male rats were treated with an antagonist of luteinizing hormone-releasing hormone (LHRH; ORG. 30276) from postnatal days 6-15. Previously, it has been demonstrated that this treatment results in delayed pubertal development, decreased testicular weight, impaired fertility and adult sexual behavior.

Acute desensitization of pituitary FSH response to LHRH in ovariectomized rats: further evidence that in the presence of ovarian proteins the LHRH-dependent, LH-like component of FSH release becomes apparent.

Pulsatile release of LHRH and short-term pituitary desensitization to LHRH in the rat are believed to be necessary for the maintenance of LH pulsatility. In contrast, FSH release is partly induced by LHRH release and is partly LHRH-independent. This LHRH-independent release of FSH is subject to inhibitory feedback control by ovarian proteins (probably inhibin), and may obscure an LHRH-induced short-term loss of pituitary FSH responsiveness to LHRH.

Regulation by ovarian factors of the LHRH-induced LH response in pituitary glands in situ or grafted under the kidney capsule in intact and ovariectomized rats.

When pituitary glands from intact female rats are incubated with LHRH, the resulting LH release shows a biphasic pattern: an initial low rate of LH release (lag phase) is followed by a high rate. When pituitary glands from long-term ovariectomized rats are incubated, the rate of LH release is high throughout stimulation with LHRH. The disappearance of the lag phase might be due to increased LHRH release after ovariectomy and/or the disappearance of ovarian factors.

Administration of a GnRH-antagonist to immature rats affects subsequent female and male pubertal development differently.

Gonadotropin secretion was inhibited in immature male and female rats by sc administration of the GnRH-antagonist ORG30276 (GnRH-A) on days 6, 9, 12 and 15. In GnRH-A-treated females this resulted in suppression of the temporarily increased plasma LH and FSH levels, which normally occur in prepubertal female rats. Ovarian weight was decreased.

Pulsatile LH-RH treatment induces a relatively low response of LH and FSH, while discontinuation enhances the response in women with amenorrhea of suprapituitary origin.

Five women with amenorrhea of suprapituitary origin were given intravenous injections of 10 micrograms LH-RH every 90 minutes for 4 days by means of a portable infusion pump. Immediately before and after this, the LH and FSH responses to a test dose of 100 micrograms LH-RH were measured. Four days after discontinuation of the treatment, so that LH and FSH could be measured, blood was sampled every 10 minutes for a period of 6 hours, during which 20 micrograms LH-RH was injected intravenously every hour.

Pulsatile GnRH treatment of the ovariectomized rat and release of LH and FSH.

The effect of pulsatile GnRH administration on the levels of LH and FSH was investigated in rats that had been ovariectomized 2 weeks earlier. Also the asynchronous occurrence of endogenous and GnRH-induced LH and FSH pulses was analysed. A small pulse dose of GnRH (1.

The influence of pulsatile GnRH administration to the ovariectomized rat on the pituitary response to GnRH and the occurrence of spontaneous LH pulses.

Otherwise untreated adult ovariectomized rats were given pulses of GnRH (5 ng/100 g body weight iv) once every 60 or 120 min for 24 or 96 h. On the first and last day of the experiment plasma LH was estimated during the administration of GnRH pulses. Endogenous LH pulses between exogenously generated LH pulses were observed in nearly all animals on both the first and the last day, without any change in nadir and amplitude values.

Patterns of LH and FSH in men during high-frequency blood sampling.

The aim of the study was to test the hypothesis that in serial determinations of concentrations of LH and FSH involving blood samples taken every minute, the observed pulses of LH and FSH which last less than 3-4 min might not be a physiological phenomenon but part of the 'noise' of the radioimmunoassay or blood-sampling technique. Blood was sampled every minute for a period of 90 min in six men. During the first 45 min, blood was sampled by means of vacuum tubes only.

Phenobarbital enhances pituitary LH release induced by LRH pulses in the ovariectomized rat.

In the ovariectomized (OVX) rat, the plasma LH response was measured to a pulse of LRH (1.25 or 5 ng/100 g body weight, ia) given before and 1 h after ip administration of phenobarbital (80 mg/kg body weight). The LH response to the LRH pulses was increased 1 h after phenobarbital.

Comparison of the time courses of luteinizing hormone (LH) secretion rates during continuous stimulation by LH-releasing hormone (LH-RH) in vivo and in vitro.

The patterns of LH secretion during constant stimulation of the pituitary glands of estradiol-treated ovariectomized rats with a maximally stimulating amount of LH-RH in vivo and in vitro correspond with each other qualitatively and quantitatively. In vitro the changes with time of the LH secretion rate are somewhat retarded, especially the occurrence of desensitization.

Effect of pretreatment of long-term ovariectomized (OVX) rats with a competitive LRH antagonist on FSH release in vitro.

The effect of a single sc injection of an LRH antagonist ((Ac-D-p-Cl-Phe1,2,D-Trp3,D-Phe6,D-Ala10)-LRH, Org 30093) into OVX rats on FSH release 24 h later was studied. Plasma FSH was decreased but pituitary FSH content was not changed. Incubation of the pituitary glands during 4 h resulted in a decreased basal release.

Effect of pretreatment of long-term ovariectomized rats with an LRH antagonist on LH release in vitro by LRH, elevated K+ or N6-monobutyryl adenosine 3',5'-monophosphate (mbcAMP) plus theophylline.

The effect of the LRH antagonist (Ac-D-p-Cl-Phe1,2,D-Trp3,D-Phe6-D-Ala10)LRH (Org 30093) on pituitary LH release was studied, using pituitary glands of ovariectomized rats. In vitro, the antagonist had no detectable agonist activity in the concentration used, had no effect on the maximal LH release which can be induced by LRH and shifted the dose-response line of LRH to the right, without changing its slope. By this the antagonist fulfilled the conditions of purely competitive antagonist.

Infectious (septic) arthritis of the distal intertarsal and tarsometatarsal joint in cattle.

The results of treatment of infectious (septic) bone spavin in cattle admitted to the department of large animal surgery, Utrecht University, between 1961 and 1982 are reviewed. Treatment comprised either antibiotic administration, radiation or surgery, of which the latter two methods appeared to produce better results. However, radiation of the affected area was both time consuming and expensive.

Effect of pre-treatment of long-term ovariectomized rats with anti-LRH on the response of the pituitary gland in vitro to the analogue of LRH D-ser-(tBu)6-des-gly10-ethylamide-LRH (Buserelin).

Ovariectomized rats were injected iv with an antiserum against LRH or normal rabbit serum. Anti-LRH caused a decrease of plasma LH and FSH. After 24 or 48 h, the rats were decapitated and the pituitary glands incubated in the presence of an analogue of LRH which reacts minimally with anti-LRH (Buserelin).