The effect of Δ1tetrahydrocannabinol on luteinizing hormone release in castrated and hypothalamic deafferented male rats

Summary ¹Tetrahydrocannabinol (THC) acutely suppresses tonic serum luteinizing hormone (LH) and prolactin levels in adult male rats. The exact site of its action has not been identified. We have performed complete hypothalamic deafferentation (CHD), which disrupts the medial basal hypothalamus (MBH) from the rest of the CNS, but did not abolish the abilitiy of THC to suppress hypothalamic-pituitary responses in gonadectomized male rats. This was shown by the equal reduction in serum levels of LH and prolactin in non-deafferented (ND) and CHD animals. These results indicate that THC is able to act inside the MBH and that the MBH-pituitary axis remains responsive to its inhibitory effect despite interruption of the neural connections between the MBH and extrahypothalamic areas. However, the corticotropin releasing factor neurons in the MBH appear functionally impaired as a result of the transection and become unresponsive to the normally produced THC stimulation. Different patterns of action seem to govern the various hypophyseal hormones controlled by the hypothalamus, suggesting that the release of LH releasing hormone and prolactin inhibiting factor might be maintained by the activity of neurons surviving inside the island.     

Effects of ovariectomy and steroid replacement on hypothalamic LHRH content in aging female rats

To examine the role of age on the hypothalamic LHRH response to ovariectomy (ovx) and steroid replacement, young cycling (3-4 months) and old constant estrous (18-20 months) rats were ovariectomized. Two weeks later, rats were treated for 5 days with estradiol benzoate (E, 5 micrograms/kg), progesterone (P, 10 mg/kg), E + P (5 micrograms E + 10 mg/kg) or corn oil, after which time they were killed for determination of hypothalamic LHRH content. The young and old ovx rats had similar levels of LHRH in the medial basal (MBH) and anterior (AH) hypothalamus, but E treatment was only effective in increasing MBH-LHRH content in the young animals. There was no significant effect of P alone or in combination with E. In the second experiment, similar results were seen using a single dose of E (1 microgram/rat) in young and old ovx rats. In addition, the radioimmunoassay of LHRH using two different antibodies binding to different portions of LHRH gave similar results in young and old rats, suggesting that the LHRH peptide was being processed similarly in the two age groups. In conclusion, it appears that hypothalamic LHRH content of young and old ovx rats does not differ with age despite a marked attenuation of serum LH levels with age. The hypothalamus from old rats, however, is less responsive to steroid stimulation of LHRH content.     

Evaluation of hypothalamic-pituitary-adrenal axis in amenorrhoeic women with insulin-dependent diabetes

Diabetes is associated with a higher incidence of secondary hypogonadotrophic amenorrhoea. In amenorrhoeic women with insulin-dependent diabetes a derangement in hypothalamic-pituitary-ovary axis has been proposed. No data exist on hypothalamic-pituitary-adrenal function in these women. Gonadotrophin releasing hormone (GnRH), corticotrophin releasing hormone (CRH), metoclopramide and thyroid releasing hormone (TRH) tests were performed in 15 diabetic women, eight amenorrhoeic (AD) and seven eumenorrhoeic (ED). Frequent blood samples were taken during 24 h to evaluate cortisol plasma concentrations. There were no differences between the groups in body mass index, duration of diabetes, insulin dose and metabolic control. The AD women had lower plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, oestradiol, androstenedione and 17-hydroxyprogesterone (17-OHP) than the ED women. The responses of pituitary gonadotrophins to GnRH, and of thyroid stimulating hormone (TSH) to TRH, were similar in both groups. The AD women had a lower prolactin response to TRH and metoclopramide, and lower ACTH and cortisol responses to CRH, than the ED women. Mean cortisol concentrations > 24 h were higher in the amenorrhoeic group. Significant differences in cortisol concentrations from 2400 to 1000 h were found between the two groups. Insulin-dependent diabetes may involve mild chronic hypercortisolism which may affect metabolic control. Stress-induced activation of the hypothalamic-pituitary-adrenal axis would increase hypothalamic secretion of CRH. This would lead directly and perhaps also indirectly by increasing dopaminergic tonus to inhibition of GnRH secretion and hence hypogonadotrophic amenorrhoea. Amenorrhoea associated with metabolically controlled insulin-dependent diabetes is a form of functional hypothalamic amenorrhoea that requires pharmacological and psychological management.     

Gonadotrophin secretion in the ovariectomized guinea-pig: effects of electrical stimulation of the hypothalamus and of LH-RH.

1. Serial blood samples were collected from anaesthetized spayed guinea-pigs subjected to anterior hypothalamic stimulation or injected with luteinizing hormone-releasing hormone (LH-RH), and the effect on the secretion of follicle-stimulating hormone (FSH) and LH followed. 2. Hypothalamic stimulation enhanced LH secretion, although the response waned during the course of the 1 hr period of stimulation; the secretion of FSH was not increased. After stimulation, FSH and LH levels fell below control values. 3. The response to stimulation of the hypothalamus was greater 2 weeks after spaying than after 1 week. 4. Since repeated periods of hypothalamic stimulation induced repeated surges of LH secretion, the decline in LH secretion during stimulation was not likely to have resulted from hypothalamic damage, while the observation that the plasma concentration of FSH and LH declined below control values after brain stimulation implies the operation of inhibitory mechanisms. 5. Pre-treatment of spayed guinea-pigs with progesterone depressed the resting plasma concentration of LH but did not affect the immediate response to hypothalamic stimulation. After hypothalamic stimulation the plasma gonadotrophin levels did not fall below control values. 6. Pre-treatment with oestradiol benzoate depressed the resting plasma level of LH and slightly reduced the size of the LH surge produced by hypothalamic stimulation. However, the raised plasma LH concentration was sustained after stimulation ended. 7. The response to hypothalamic stimulation after pre-treatment with progesterone and oestradiol benzoate showed features of the reaction to each steroid given singly. 8. The I.V. injection of 0-5 microng LH-RH induced a surge of LH secretions without affecting FSH discharge. 9. Pre-treatment with progesterone did not greatly modify the response to LH-RH but after an injection of oestradiol the high level of LH produced by the releasing factor was sustained for about 2 hr. 10. Injections of LH-RH during the phase of depressed LH release after hypothalamic stimulation produced a surge of LH secretion which matched that seen in non-stimulated animals.     

Sexual dimorphism in the effects of mating on the in vitro release of LHRH from the ferret mediobasal hypothalamus.

A sexually dimorphic pattern in the secretion of luteinizing hormone (LH) has previously been shown to occur in response to mating in an induced ovulating species, the ferret, with mating augmenting the secretion of LH in females but not in males. The aim of this study was to determine whether this dimorphic pattern in the postcoital secretion of LH reflects a dimorphic effect of mating on the neural release of luteinizing hormone releasing hormone (LHRH). The effect of mating on the in vitro release of LHRH from mediobasal hypothalami (MBH) collected from breeding male and female ferrets was studied. Luteinizing hormone releasing hormone release and content were significantly reduced in tissues from estrous females sacrificed 0.25 h after mating compared to unpaired estrous females and estrous females sacrificed 1 or 2.6 h after the mating stimulus. By contrast, the release of LHRH from MBH fragments and LHRH tissue content were equivalent in breeding males that were sacrificed 0.25 h after mating and in breeding males that were left unpaired. These data suggest that the postcoital surge of LH in the female ferret is preceded by a release of LHRH that initially depletes neuronal terminals within the MBH, whereas LHRH release, like pituitary LH secretion, is minimally affected by mating in males.     

Mechanism of the onset of puberty, with special reference to the dynamics of the hypothalamic gonadotropin releasing factor and pituitary gonadotropin

In vivo and in vitro studies of the dynamics of hypothalamic FSH-RF, LH-RF, PIF, and anterior pituitary FSH, LH, and prolactin during the process of sexual maturation were carried out in female Wistar-starin rats. Around the time of vaginal opening there was a wide fluctuation of hormonal values. The peak of FSH content in the anterior pituitary was on Day 25 after birth, LH peaked on Day 40, and prolactin on Day 45. Addition of crude HE (hypothalamic extract) of 20-45 day old female rats to the incubation fluid of anterior pituitary glands resulted in a rise of FSH and LH activity in the culture fluid. The greatest increase of FSH activity was seen on the addition of HE of 20-day-old rats. LH increased most on hte addition of HE in 35-day-old rats and prolactin decreased on the addition of HE in 45-day-old rats. The relationship between anterior pituitary FSH, LH, and prolactin contents and hypothalamic RF and IF is suggested.     

Role of the preoptic brain in the regulation of preovulatory gonadotropin surges in the hamster

Summary These studies have examined the role of the preoptic-suprachiasmatic area (POA-SC) in brains of cyclic female hamsters in regulating proestrous preovulatory gonadotropin surges. The spontaneous release of LH and FSH which normally occurs on proestrous afternoon was blocked with phenobarbital. Temporal changes in serum LH and FSH were measured in such blocked animals after delivery of direct current (100 A/60 s) to the POA-SC or that portion of the medial basal hypothalamus (MBH) which includes the arcuate nuclei and the median eminence. Bilateral dc treatment of MBH resulted in a 30-fold increase in serum LH and a 4-fold rise in serum FSH over basal concentrations. Unilateral MBH dc treatment produced a 12-fold increase in serum LH but FSH levels remained basal. In contrast, the delivery of dc to the POA-SC did not evoke any increase in serum LH or FSH. Sham electrode placement in the MBH or POA-SC also did not alter basal LH and FSH serum concentrations. These results suggest that, unlike the rat, passage of dc with concomitant production of an irritative lesion and deposition of ferrous ion does not activate structures responsible for preovulatory gonadotropin surges in hamsters.In a second study, discrete electrochemical lesions were produced in the basal anterior portion of the preoptic brain. These lesions did not involve the medial preoptic area or the suprachiasmatic nuclei. Following such brain destruction, spontaneous ovulation, LH surges, and 4-day vaginal cyclicity ceased. When the suprachiasmatic nuclei or extensive regions of the dorsal medial preoptic area, including the anterior commissure, were destroyed, vaginal cyclicity was disrupted for only 8–12 days. Thereafter, these animals had spontaneous preovulatory gonadotropin surges and ovulated. Seemingly, input from the medial basal anterior preoptic region (anterior to the SC) is essential for preovulatory LH and FSH surges to occur.This research was supported by USPHS Grant HD-02138Postdoctoral Fellow, Reproductive Endocrine Training Program supported by USPHS Grant HD-00435.     

Modulation of folliculogenesis and steroidogenesis in women by graded menotrophin administration

BACKGROUND: To test the effects of progressively decreasing dosages of exogenous LH we combined various amounts of HMG, containing FSH, LH and HCG, and highly purified (HP) FSH to treat 120 GnRH agonist-suppressed infertile female patients as candidates for controlled ovarian stimulation (COS). METHODS: Subjects were randomly assigned to four treatment groups that received the following daily i.m. gonadotrophin regimens: A, FSH 150 IU only; B, FSH 150 IU and LH activity 37.5 IU; C, FSH 150 IU and LH activity 75 IU; D, FSH 150 IU and LH activity 150 IU. FSH dose adjustments were allowed only after the 14th treatment day. Monitoring included transvaginal ultrasound at 2-day intervals and daily determinations of LH, FSH, estradiol (E(2)), progesterone, testosterone and HCG. RESULTS: Duration of COS was significantly shortened in patients receiving at least 75 IU daily of LH activity. Small (<10 mm diameter) pre-ovulatory ovarian follicle occurrence was inversely correlated with LH activity dose administered (r = -0.648, P < 0.0001) and serum HCG levels (r = -0.272, P < 0.01) but not to serum LH levels. Serum testosterone levels were positively correlated to the LH activity dose administered (r = 0.313, P < 0.001), while serum progesterone levels were positively correlated to the FSH dose administered (r = 0.447, P < 0.00001) but not to the LH activity dose administered. CONCLUSIONS: Firstly, HCG content considerably contributes to HMG activity; secondly, menotrophin LH activity content can reduce in a dose-dependent manner the occurrence of small pre-ovulatory follicles; and finally, contrary to common belief, enhanced FSH stimulation rather than LH activity appears to cause premature follicle luteinization during COS.     

The origins and sequelae of abnormal neuroendocrine function in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a common clinical disorder characterized by ovulatory dysfunction and hyperandrogenaemia. A neuroendocrine hallmark of PCOS is persistently rapid LH (GnRH) pulsatility, which favours pituitary synthesis of LH over that of FSH and contributes to the increased LH concentrations and LH : FSH ratios typical of PCOS. Inadequate FSH levels contribute to impaired follicular development, whereas elevated LH levels augment ovarian androgen production. Whereas luteal phase elevations in progesterone normally slow GnRH pulse frequency, women with PCOS do not experience normal progesterone-mediated slowing, due in part to impaired hypothalamic progesterone sensitivity. This reduction in hypothalamic progesterone sensitivity appears to be mediated by elevated androgens because sensitivity can be restored with the androgen receptor blocker flutamide. The ovulatory and hormonal abnormalities associated with PCOS generally present during puberty, typically associated with hyperandrogenaemia. Along with elevated LH concentration and pulsatility, some girls with hyperandrogenaemia have impaired hypothalamic progesterone sensitivity similar to that seen in adult women with PCOS. We propose that peripubertal hyperandrogenaemia may lead to persistently rapid GnRH pulse frequency via impaired hypothalamic feedback inhibition. The subsequent abnormalities in gonadotropin secretion, androgen production and ovulatory function may support progression towards the adult PCOS phenotype.     

Protein kinase C (PKC) activity and PKC messenger RNAs in human pituitary adenomas.

Protein kinase C (PKC) is involved in the differentiation and growth regulation of a variety of tissues including anterior pituitary gland cells. To determine the distribution of PKC in different types of adenomas, PKC activity was analyzed in human pituitary tumors and the effects of hypothalamic hormone stimulation on PKC activity were examined in cultured adenoma cells. Gonadotroph (LH/FSH) and null cell adenomas had significantly higher levels of particulate, soluble, and total PKC activity compared with growth hormone (GH) adenomas (P < 0.05). Chronic stimulation of null cell adenomas with gonadotropin hormone-releasing hormone or of one GH adenoma with GH-releasing hormone for 7 days did not significantly alter total PKC activity in pituitary cells cultured in serum-free medium. Localization of the calcium-dependent PKC isozymes (alpha, beta and gamma) by immunohistochemistry and in situ hybridization revealed predominantly PKC alpha in all adenomas and variable expression of PKC beta and gamma in some tumors. When the calcium-independent PKC isozymes (delta, epsilon, and zeta) were localized by in situ hybridization, normal and neoplastic pituitaries expressed abundant mRNA for PKC epsilon, whereas some tumors and one normal pituitary had a few cells positive for PKC zeta mRNA as evaluated by grain density and the number of cells labeled. These results indicate that there is a variable distribution of PKC mRNA isozymes in human pituitary adenomas and that normal pituitaries and pituitary adenoma cells express the mRNA for both the calcium-dependent and some of the calcium-independent PKC isozymes. Chronic treatment with the hypothalamic gonadotropin hormone-releasing hormone and GH-releasing hormone, which increased LH/FSH and GH secretion, respectively, did not increase PKC activity in cultured adenoma cells. The presence of calcium-dependent and calcium-independent PKC isozymes in normal and neoplastic pituitary cells indicates that PKC probably plays a major role in signal transduction in the human pituitary adenomas examined in this study.     

Prolactin and gonadotrophin dynamics in response to antagonists of LHRH and dopamine in ovariectornized rhesus monkeys: a dissection of their common secretion

This experiment was designed to study the prolactin (PRL) andgonadotrophin response to an inhibitory analogue of luteinizinghormone releasing hormone (LHRH-A; ORG 30276) and a dopamineantagonist, metoclopramide (MCP), in castrated female rhesusmonkeys. The LHRH-A given as an i.v. bolus followed by an Infusion2 h later induced a significant decline in circulating PRL levelsreaching a maximum suppression 1 h after initiation of the LHRH-Ainfusion. Intravenous administration of MCP, performed 1 h afterbegining the LHRH-A infusion, resulted in a prompt and abruptrise in PRL levels in the LHRH-A group as well as in the controls.Luteinizing hormone (LH) and follicle stimulating hormone (FSH)levels showed a progressive decline during LHRH-A treatment.Injection of MCP did not affect the levels of LH and FSH ineither of the groups. The data obtained demonstrate in primatesthat the prolactin inhibitory effect of LHRH-A is easily overcomeby the dopamine antagonist, MCP, whereas the LHRH-A-inducedgonadotrophin suppression remains unaffected by MCP.     

Rapid inhibitory effects of an LHRH agonist implant on the oestrogen-induced LH surge and the induction of a defective luteal phase after an agonist-induced ovulation in the macaque

Three experiments were performed to evaluate in detail pituitary--ovarian function during the first 21 days after treatment with a luteinizing hormone releasing hormone (LHRH) agonist implant. First, six adult macaques with normal menstrual cycles received an LHRH agonist implant during the late luteal or early follicular phase. To investigate the rapidly of effects on pituitary responsiveness the macaques were treated with 50 micrograms LHRH at the time of implant (day 0) and at days 4, 10 and 21. Effects on serum LH and FSH were determined on basal samples and at 30 and 60 min. At 4 days, LH and FSH were elevated as a result of the implant and no further response to LHRH challenge was observed. By 10 days, LH had returned to the pretreatment range but was unresponsive to the LHRH challenge; by 21 days, LH was lower than the pretreatment range and again LHRH failed to induce a significant response. Serum FSH concentrations also declined during treatment, but in contrast to LH, a significant response to LHRH was observed on day 10. Secondly, the ability to respond to an oestrogen provocation test was examined in six macaques with normal menstrual cycles treated with the LHRH agonist implant during the late luteal or early follicular phase and 7 days later with 50 micrograms/kg oestradiol benzoate in oil s.c. to induce an LH/FSH surge. In control animals, oestrogen treatment resulted in a positive feedback surge, reaching a maximum at 48 h post-injection. In contrast, agonist-treated animals showed complete abolition of the expected increase in LH and FSH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypothalamic-pituitary axis during reproductive aging in mice

We correlated the content of hypothalamic (HT) GnRH and pituitary (PT) GnRH receptor sites with PT and plasma gonadotropin levels throughout aging in C57BL/6J mice. Female mice of 4-6 months (young), 10-12 months (middle-age) or 15-18 months (old) of age were studied either intact or 15 days post-ovariectomy (OVX) with or without E2 therapy. In intact mice, HT GnRH content increased twofold during aging while GnRH receptor sites in PT remained unchanged. PT content of both FSH and LH gradually rose during aging while plasma concentration rose even more. OVX resulted in a significant decrease in both HT GnRH content and PT receptor sites and no age difference was observed. OVX also resulted in a significant increase in both PT content and plasma levels of gonadotropin in young and middle-age mice while old mice showed a blunted response. After E2 therapy for 7 days, HT GnRH content and PT GnRH receptor sites returned to normal levels in all age groups. By contrast, E2 therapy resulted in no change in PT content of FSH:LH in any age group. Whereas plasma FSH:LH levels returned to intact levels in young mice, they remained elevated to OVX levels in middle-age and old ones. Our results demonstrate an age related dichotomy in the PT production of FSH:LH unrelated to changes in either HT GnRH content or its PT receptor sites, thus suggesting cellular defects in post-receptor binding events within the pituitary.     

Psychoendocrine response to sexual arousal in human males

The hypothesis is tested that luteinizing hormone (LH) and follicle stimulating hormone (FSH( may be released from the anterior pituitary in response to a psychological state of sexual arousal. LH levels in 10 male volunteers were found to be higher after viewing a sexually arousing film than after a control film. The magnitude of LH response was found to be positively correlated with the subjective evaluation of sexual arousal. FSH levels tended in the same direction bu the predominant and unexpected finding for this hormone was that levels were consistently lower during the first session, when anxiety was high, and higher during the second session, when anxiety was less, whether control or stimulus film had been shown. This study is analogous to those demonstrating the responsiveness of other anterior pituitary hormones to specific psychological states.     

浙江省台州地区167例男性不育的染色体畸变及生殖激素水平研究

目的研究男性不育与染色体畸变及生殖激素水平关系。方法对167例男性不育患者进行染色体核型分析和精液常规检测,用电化学发光法测定生殖激素水平。结果不育男性患者染色体异常发生率为10.8%(18/167),其中性染色体异常占7.2%(12/167),常染色体异常占3.6%(6/167)。染色体核型异常患者FSH、LH均不同程度升高,而T水平偏低;染色体核型正常无精子症组FSH、LH显著高于少弱精子症与对照组,少弱精子组也显著均高于对照组,另四项T、PRL、E2、P三组间不存在差异。结论染色体异常是造成男性不育重要因素,而生殖激素水平能反映不同程度的生精障碍,对男性不育者有必要进行细胞遗传学检查和生殖激素检测。     

Follicle-stimulating hormone as a prognostic indicator in clomiphene citrate/human menopausal gonadotrophin-stimulated cycles for in-vitro fertilization

Follicle-stimulating hormone (FSH), luteinizing hormone (LH), oestradiol and prolactin levels were studied in a sequential clomiphene citrate/human menopausal gonadotrophin (CC/HMG) regimen for in-vitro fertilization. At completion of CC administration, the median FSH level in 44 cancelled cycles was elevated compared to a control group of 65 completed cycles, 29 IU/l versus 15 IU/l, P less than 0.01. Also the median FSH/LH ratio was higher in the cancelled cycles than in the control group, 1.08 versus 0.71, P less than 0.05. Conversely, the median oestradiol level was lower in the cancelled cycles than in the completed cycles, 0.27 nmol/l versus 0.59 nmol/l, P less than 0.01. No difference was seen in the median LH and prolactin levels. An FSH value above the 95% confidence limit was found in 24 of the cancelled cycles, but in only two of the completed cycles. Based on this study, an elevated FSH value following CC administration predicts a poor response to further stimulation with an accuracy of 92.3% and should result in cancellation of the cycle.     

Effects of atrial natriuretic factor on anterior pituitary hormone secretion in normal man

Summary The effects of intravenous human atrial natriuretic factor ANF(99-126) administration on anterior pituitary hormone secretion have not been extensively investigated in humans. We repeatedly studied 10 healthy volunteers (5 female, 5 male, aged 28±2 years) on 2 occasions, 3 days apart. In randomized, single blind order, subjects received pretreatment with either placebo or intravenous ANF(99–126) (bolus 100 g/kg, 30-min infusion of 0.1 g/kg-min). Subsequently, on both occasions subjects received a combined intravenous bolus injection of pituitary releasing hormones (200 pg thyrotropin releasing hormone, 100 g gonadotropin releasing hormone, 50 g growth hormone releasing hormone and 100 g human adrenocorticotropin releasing hormone; Bissendorf, Hannover, FRG). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), thyrotropin (TSH), prolactin, ANF and cyclic guanosine monophosphate (GMP) were determined by radioimmunoassay. ANF(99–126) treatment induced a significant reduction in basal ACTH plasma concentrations and tended to decrease basal plasma cortisol. The TSH response to combined releasing hormone administration was significantly diminished after ANF(99-126) pretreatment. In women, the releasing hormone induced prolactin increase was reduced after ANF(99–126) pretreatment. With the present study design, ANF(99–126) did not alter the basal or releasing hormone stimulated plasma concentrations of cortisol, LH, FSH and GH. Releasing hormone administration did not affect ANF and cyclic GMP plasma levels. In humans, effects of natriuretic peptides on anterior pituitary hormone secretion may have to be considered with investigational or therapeutic administration of ANF analogues or agents interfering with the ANF metabolism.Abbreviations ANF(99–126) human atrial natriuretic factor - ACTH adrenocorticotropic hormone - LH luteinizing hormone - FSH follicle-stimulating hormone - GH growth hormone - TSH thyrotropin - PRL prolactin - cyclic GMP cyclic guanosine monophosphate - TRH thyrotropin releasing hormone - GnRH gonadotropin releasing hormone - GHRH growth hormone releasing hormone - CRH adrenocorticotropin releasing hormone     

Exercise and gonadal function

Exercise is associated with release of a number of pituitaryand hypothalamic hormones and a decline in the concentrationof luteinizing hormone (LH). Follicle stimulating hormone (FSH)is generally not influenced by exercise. Serum inhibin concentrations,which are reciprocally influenced by serum FSH concentrations,are increased in some animals but are unchanged after acuteexercise in human males. Teleologically, the decline in gonadotrophichormone (LH) secretion after exercise may be geared to enhanceindividual survival over species propagation in times of stress,analogous to the postulated ‘fight or flight’ reaction.The decrease in gonadotrophic hormone (LH) secretion is believedto be due to changes in gonadotrophin releasing hormone (GnRH)pulse frequency and amplitude, particularly in women, who oftendevelop amenorrhoea. Males have less dramatic changes in theirhypothalamic—pituitary—gonadal axis, although asignificant decrease in serum testosterone in physically conditionedmales can usually be demonstrated. In this update possible mechanismsfor the decline in gonadotrophin secretion with exercise arebriefly discussed.     

不孕症患者性激素水平的变化

为了解性激素的变化在不孕症发病过程中的作用,将84例患不孕症的妇女,分为四组,在卵泡期对血清六项激素：FSH、LH、PRL、E2、T、P进行了放射检测。检测结果表明：四组患者的六项指标均高于标准值,除E2（P＜0．05）外,其他各项指标的组均数间无显著性差别,在被检病例中E2、P含量增高的患者所占的百分比与LH／FSH比值增高患者所占的百分比基本一致。     

Serum anti-Müllerian hormone is more strongly related to ovarian follicular status than serum inhibin B,estradiol, FSH and LH on day 3

BACKGROUND: The study aim was to compare the relationship between serum anti-Müllerian hormone (AMH) levels and other markers of ovarian function with early antral follicle count on day 3. METHODS: A total of 75 infertile women was studied prospectively. On cycle day 3, serum levels of AMH, inhibin B, estradiol (E(2)), FSH and LH levels were measured, and the number of early antral follicles (2-10 mm in diameter) estimated at ultrasound scanning to compare the strengths of hormonal-follicular correlations. RESULTS: Median (range) serum levels of AMH, inhibin B, E(2), FSH and LH were 1.39 ng/ml (0.24-6.40), 90 (16-182) pg/ml, 31 (15-111) pg/ml, 7.0 (2.9-19.3) mIU/ml and 4.7 (1.2-11.7) mIU/ml respectively, and follicular count was 12 (1-35). Serum AMH levels were more strongly correlated (P < 0.001) with follicular count (r = 0.74, P < 0.0001) than were serum levels of inhibin B (r = 0.29, P < 0.001), E(2) (r = -0.08, P = NS), FSH (r = -0.29, P < 0.001) and LH (r = 0.05, P = NS). CONCLUSIONS: Serum AMH levels were more robustly correlated with the number of early antral follicles than inhibin B, E(2), FSH and LH on cycle day 3. This suggests that AMH may reflect ovarian follicular status better than the usual hormone markers.