雌二醇对动情间期切除卵巢母羊黄体生成激素脉冲分泌的抑制作用

12只动情间期母羊切除卵巢后,根据随机皮下植入或不植入E_2而分为二组。通过颈静脉插管每5～10分钟采血一次,连续8～9小时,分离血浆作LH放免测定。实验组的平均LH基础分泌水平和LH脉冲幅高比对照组显著减低,LH脉冲频率无明显改变。LH的平均基础分泌水平和脉冲幅高显著相关。本研究表明,植入E_2抑制垂体LH的分泌,其作用可能主要是抑制LH对GnRH的反应,因此,作用部位是在垂体水平。LH基础分泌水平的下降,亦可能是E_2的抑制作用所致。     

可乐宁与纳洛酮对垂体前叶激素的影响

阿片受体拮抗剂纳洛酮能促进LH和FSH的释放,可乐宁具有同样作用。吗啡抑制LH分泌的作用亦被可乐宁阻断。由此表明阿片能神经和去甲肾上腺素能神经对垂体前叶激素水平有相互作用。为     

促性腺激素过高患者经长效LH-RH类似物刺激后的血清促性腺激素浓度

健康男子静注作用较长的LRH类似物D-丝(叔丁)~6去甘酰胺~(10)-LRH后60分钟内血清LH浓度最高,但在健康妇女中,LH峰值延迟到240分钟以后,这种LH释放的性别差异,在女性不受血清雄激素浓度增加的影响,在男性则不受血清E_2浓度增加的影响,可能由于男女LH“第二储备”     

GnRH/EGFP转基因对雌性大鼠黄体生成素分泌的影响

目的探讨GnRH/EGFP转基因对雌性大鼠黄体生成素(LH)分泌的影响。方法建立GnRH/EGFP转基因雌性大鼠,采用重复取静脉血样的方法测定其LH的分泌水平,评价GnRH/EGFP转基因对雌性大鼠黄体生成素分泌的影响。结果非转基因对照大鼠的脉冲式LH的分泌较转基因雌性大鼠的LH分泌更明显。两组大鼠的平均LH浓度和LH脉冲幅度无明显差异,但是转基因雌性大鼠的LH脉冲频率明显低于雌性对照组大鼠(P<0.05)。激素诱导和交配诱导均可引起GnRH峰,说明脉冲频率的减少并不能反映雌性大鼠激素分泌对其整体的影响。结论雄性大鼠正常的间断性激素分泌可能本质上并非是由于EGFP在神经元中的表达,这可能是多种内部和外部因素共同作用的结果,其中一些内部或外部因素可能是调节激素搏动性分泌的主要因素。     

雌性大鼠促黄体生成素分泌的老年性变化——下丘脑前列腺素E_2的作用

为了确定下丘脑前列腺素E_2(PGE_2)调节雌性大鼠促黄体生成素(LH)分泌的作用是否存在年老性变化,本实验首先用放射受体法测定4～5,15～16和20～21月龄(mo)不同生殖状态大鼠的血清LH基础水平,接着,向这些大鼠的侧脑室内输注PGE_2,比较不同年龄和不同生殖状态大鼠的LH对     

外侧下丘脑损伤地纳络酮刺激黄体激素释放的影响

β-内啡肽及其拮抗剂纳络酮对黄体激素(LH)释放的作用已被确认。鸦片样肽的作用可能是通过激发黄体激素释放因子(LHRF),但目前还不清楚它是对下丘脑LHRF神经元的直接作用,抑或是其机制涉及到其它神经递质系统。为了阐明此系统的作用,作者观察了上行去甲肾上腺素(NA)能通路对LH纳络酮刺激作用。     

老年人群血清LH、PRL及睾酮变化规律的研究

应用RIA方法．检测627例血清睾酮（T）、促黄体生成素（LH）和泌乳素（PRL）水平．探讨各激素的增龄性变比。结果表明：血清T水平对照组为32．07±14．25nmol／L其它各组随增龄呈进行性降低．且与对照组相比存在显著差异（P＜005）：血清LH水平是随龄增高趋势．且与T变比呈显著负相关（r=－0．21，P＜0．01）。血清PRL水平亦呈现随龄增高趋势。PRL与T（r=－0．12．P＜0.05）、PRL与LH（r=0．11．P＜0．05）呈微弱相关关系。上述结果提示．在男性衰老过程中．T水平逐渐降低．对LH负反馈抑制作用减弱，而引致LH分泌增高．血清PRL对性腺轴激素水平有影响．但其具体作用及作用方式有待进一步研究。     

系统性红斑狼疮患者血清性激素水平的研究

目的探讨性激素在系统性红斑狼疮(SLE)发病及病程中的作用。方法测定33例SLE患者血清雌二醇(E2)、孕酮(P)、睾酮(T)、黄体生成素(LH)、卵泡刺激素(FSH)、泌乳素(PRL)的水平。对照组采用年龄、性别和卵巢周期与病例组1:1配对的原则。结果SLE整体组及活动组,PRL均显著升高(P<0.01),LH与T均显著降低(P<0.01)。FSH与LH,LH与PRL存在高度相关性(P<0.01或0.05)。FSH和T对SLE活动性评分的价值最大。结论SLE患者血清中LH与T降低与病情活动有关;对SLE活动评分最有价值的性激素为FSH和T。     

光子治疗对胰岛素注射相关性皮下脂肪增生的影响

目的探讨光子治疗对胰岛素注射相关性皮下脂肪增生(LH)的影响。方法选取2021年4月至2022年2月于南京医科大学第一附属医院内分泌科住院的99例糖尿病并伴有LH的患者作为研究对象。测量所有患者LH长径、宽径和深径并收集其最大LH、总LH和平均LH的长、宽及深径。借助SPSS 26.0软件生成随机数字并将研究对象分为试验组(50例)和对照组(49例)。对照组接受常规护理并避免在LH部位注射胰岛素, 试验组在对照组措施的基础上开展光子治疗, 每日2次, 每个LH部位每次治疗20 min。采用两独立样本t检验、Mann-WhitneyU检验、配对样本t检验、Wilcoxon符号秩和检验比较干预前后两组患者最大LH、总LH和平均LH的长、宽及深径的组间和组内差异。结果试验组与对照组分别有3例和2例患者失访, 最终2组均纳入47例患者。在试验组和对照组, 干预后最大LH、总LH和平均LH的长径、深径及宽径较干预前均更小(均P<0.05)。干预后, 试验组最大LH和平均LH深径较对照组均更小(均P<0.05)。与对照组相比, 试验组干预前后最大LH长径、最大LH宽径、总LH长径、总L...     

胰岛素样生长因子Ⅰ对儿童青春发育启动的作用

目的探讨胰岛素样生长因子Ⅰ(IGFⅠ)对正常儿童青春发育启动的可能作用。方法对北方大庆地区526名(男266,女260)健康的6～16岁小学和中学生进行4年的连续观察和研究。每年由相同的内分泌科医师进行体检,检查第二性征的发育,并按Tanner分期法行青春发育分期。同时采血用放射免疫测定或酶联免疫分析法测定血清LH、IGFⅠ和IGF结合蛋白3(IGFBP3)的水平。按年龄和青春发育分期分析血清LH和IGFⅠ、IGFBP3在青春发育过程中的变化及其关系。结果在儿童期不论是男孩还是女孩,随着年龄的增长,血清LH和IGFⅠ、IGFBP3水平有相似的升高趋势。男孩和女孩血清LH水平与IGFⅠ和IGFBP3水平都明显相关(均P<0.01)。血清IGFⅠ水平的开始明显升高在8岁,而LH水平的明显升高在10岁,表明血清IGFⅠ水平的升高要比LH升高早2年。以青春发育期进行分析,女孩在青春发育2期血清IGFⅠ水平明显高于1期,也早于LH水平升高(3期)。男孩则显示血清LH、IGFⅠ和IGFBP3水平在2期同时升高。结论儿童期循环中血清IGFⅠ水平的升高早于LH水平的升高,提示IGFⅠ可能是调节儿童青春发育启动的外周因素之一。     

Uninephrectomy inducing quantitative and qualitative changes in LH isoforms in the male rat

Recent findings that LH stimulates renal growth have prompted us to examine whether LH exercises renotropic effects on the growing kidney following uninephrectomy. Intact (not castrated) male rats were used for sham uninephrectomy to induce surgical stress suppressing plasma LH and testosterone levels. Compared to sham surgery, uninephrectomy caused a transient 240% increase in plasma LH with a transient increase in plasma testosterone (80%) and in prostate weight on day 2. Although pituitary LH content did not change, chromatofocusing of pituitary extract revealed changed distribution patterns among seven LH isoforms, suggesting selective synthesis or secretion of LH isoforms. Castrated rats were then used so that surgical stress did not affect LH. Uninephrectomy caused sustained increases in plasma LH levels (60-110% increase) for up to six days. Three days after uninephrectomy, pituitary LH content increased significantly (30% increase) with a change in chromatofocusing profiles of LH isoforms. Plasma and pituitary FSH levels did not change. In summary, uninephrectomy changed LH isoforms quantitatively and qualitatively. These changes imply a change in gonadotropic and renotropic activities of LH after uninephrectomy.     

Preferential release of bioactive luteinizing hormone in response to endogenous and low dose exogenous gonadotropin-releasing hormone pulses in man

We used the rat interstitial cell testosterone (RICT) bioassay to assess biological LH activity secreted in response to endogenous and low dose exogenous GnRH pulses in normal men. The absence of nonspecific plasma effects in the LH bioassay was demonstrated by the finding of undetectable levels of LH bioactivity despite low but measurable immunoactivity in 10 hypogonadotropic men. Moreover, bolus injections of human LH in 6 hypogonadotropic men defined a curvilinear relationship between plasma bioactive and immunoactive LH concentrations, in which the extrapolated concentration of plasma bioactive LH at a zero dose of immunoactive LH was indistinguishable from zero. Zero bioactive LH intercepts were also found when physiological bio- and immunoactive LH concentrations derived from 7 intensively sampled normal men were subjected to linear regression using 2-dimensional error fitting. In these men, exogenous low dose (10 micrograms) iv GnRH administration resulted in preferential release of bioactive LH, with a consequent significant increase in the median plasma bio- to immunoactive (bioimmuno) LH ratio. This pattern mimicked that of endogenous LH pulsatility, in which median intrapulse bio:immuno LH ratios were significantly higher than median interpulse ratios in the same individuals (P = 0.006). Increases in spontaneous plasma bio:immuno LH ratios were not attributable to spurious rises in bioactive LH concentrations associated with decreases in serum immunoactive LH levels. Rather, sample cross-correlation analyses demonstrated positive correlations between bio- and immunoactive LH at lags of 0-40 min, indicating that both hormones increased or decreased concomitantly. These results demonstrate that LH is secreted physiologically in pulses of increased biological activity, presumably reflecting the release of a functionally compartmentalized LH pool relatively enriched in biologically active hormone. Accordingly, evaluation of the plasma bio:immuno LH ratio can provide a useful and sensitive index of qualitative changes in the LH molecule in response to endogenous (spontaneous) and exogenous GnRH stimulation.     

A decline in endogenous opioid influence during the steroid-induced hypersecretion of luteinizing hormone in the rat

Studies were undertaken to evaluate the influence of endogenous opioid peptides (EOP) on the LH hypersecretion induced in ovariectomized rats by estradiol benzoate (EB) or EB plus progesterone (EBP). Naloxone (0.1-15.0 mg/kg) was injected before (1200 h) and during (1400 and 1530 h) the LH surge induced by EBP treatment and during the LH surge after EB treatment (1600 h). The opiate antagonist readily stimulated LH secretion before the LH surge in EBP-treated rats at 1200 h and during the LH surge in EB-treated rats at 1600 h, but was much less effective during the LH hypersecretion induced by EBP treatment at 1400 and 1530 h. This decline in the LH secretory response to naloxone during the EBP-induced LH surge was not due to changes in the response of pituitary to LHRH. These studies indicate that during the period of LH hypersecretion induced by the sequential administration of EB plus P, the influence of EOP neuronal systems on LH secretion is diminished. Thus, EOP neurons may play a role in the timing and magnitude of the LH surge in EBP-treated rats.     

Interdependence of oestradiol and 5 alpha-dihydrotestosterone in modulating LH and FSH secretion in rats

The effects of oestradiol, 5 alpha-dihydrotestosterone (DHT) and oestradiol plus DHT on pituitary responsiveness to LHRH were studied. Rats ovariectomized for 2 weeks were infused s.c. (by osmotic minipump) with LHRH at 250 ng/h for 6 days. Control rats received a sham s.c. pump. On day 3, silicone elastomer implants containing oestradiol or DHT were implanted s.c. and on day 6 the effects of these in-vivo treatments on pituitary LH and FSH content and on in-vitro (perifusion) LH and FSH secretion following maximal LHRH stimulation (1 microgram/ml perifusion medium) were assessed. Luteinizing hormone-releasing hormone alone decreased pituitary LH/FSH content and, in response to acute LHRH challenge in vitro, the absolute rate of LH/FSH release, but not LH/FSH release expressed as a fraction of pituitary content. Oestradiol alone increased pituitary LH/FSH content and LHRH-induced LH/FSH release in vitro, both absolutely and as a fraction of pituitary LH/FSH. Oestradiol exacerbated the decrease in pituitary LH/FSH caused by LHRH pretreatment in vivo, and decreased the absolute rate of LHRH-stimulated LH/FSH release in vitro, but increased this rate when it was expressed as a fraction of pituitary LH/FSH. In both LHRH-treated and control rats, DHT increased pituitary LH/FSH content, did not change the absolute rate of LH/FSH release in response to acute LHRH challenge in vitro, but decreased the rate of LH/FSH release expressed as a fraction of pituitary LH/FSH content.(ABSTRACT TRUNCATED AT 250 WORDS)     

Developmental changes in the luteinizing hormone secretory pattern in peripubertal female rhesus monkeys: comparisons between gonadally intact and ovariectomized animals

Developmental changes in LH release patterns were observed longitudinally in female rhesus monkeys at 10-65 months of age. The average ages of menarche and first ovulation in this experiment (n = 14) were 31.1 +/- 2.6 and 47.0 +/- 2.6 months (mean +/- SE), respectively. To assess the ovarian influence on developmental changes in LH, data were simultaneously obtained from neonatally ovariectomized animals at similar ages. The estimation of circulating LH was made with RIA as well as biological assay. During the prepubertal period (10-20 months of age), basal LH was very low, and there was no circadian fluctuation of LH in gonadally intact monkeys. During the early pubertal stage (20-30 months of age), before menarche, basal LH levels started to increase, and a circadian LH rhythm (nocturnal increases) appeared. At the midpubertal stage (30-50 months of age), a period between menarche and first ovulation, basal LH levels further increased, and the circadian LH rhythm was maximal. At the late pubertal stage (50-60 months of age), a period after the first ovulation during which the animals were not able to reproduce fully as adults, basal LH declined, and the circadian rhythm diminished. Similar but more exaggerated developmental changes in basal LH and the circadian fluctuation of LH were observed in females ovariectomized neonatally. Basal LH levels at 10-20 months were as low as those in intact animals with no circadian rhythm present. During the early pubertal period, a circadian fluctuation appeared at the time when a slight increase in the basal LH level occurred. Furthermore, the amplitude of circadian fluctuation (the difference between morning and evening LH values) increased linearly with the increase in basal LH during the midpubertal stage. These LH parameters in ovariectomized animals reached their peaks at 40-44 months, an age before the first ovulation in intact animals. As basal LH levels declined during the late pubertal stage to postpubertal stage, circadian fluctuation disappeared. The results suggest that the increase in LH output and concomitant circadian fluctuations occur in close association with the pubertal process, and this change in LH release is not dependent on the presence of the ovary. Therefore, we suggest that alteration of the LHRH release pattern during maturation, as reflected by LH release, rather than resetting of the gonadostat, is the key factor involved in the mechanism of the onset of puberty.     

Role of mucosal microcirculation in gastric lesions induced by lateral hypothalamic lesions in rats

To evaluate the pathophysiology underlying gastric mucosal lesions induced by lateral hypothalamic (LH) lesions, we investigated the changes in acid secretion, gastric mucosal blood flow, gastric mucus and mucosal integrity in the corpus during the 4 h period and 48 h after the production of bilateral electrolytic LH lesions in male Sprague-Dawley rats. Gastric mucosal lesions were macroscopically produced 24 h (63%) and 48 h (83%) after LH lesions, although there were no visible lesions at 7 h. Gastric acid secretion was significantly increased 48 h after LH lesions, compared with that in the control group. Gastric mucosal blood flow and transmucosal potential difference (PD) in the LH lesion group immediately decreased after LH lesions and did not recover during 4 h and at 48 h. On the contrary, in the control group, gastric mucosal blood flow decreased after the brain surgery but soon recovered, and there was no significant change in PD. LH lesions resulted in the reduction of intramucosal mucus to 50% 3 h after LH lesions. Moreover, we exposed the stomach to 10 mmol/L taurocholic acid (TCA) 3 h after LH lesions to examine the disruption in gastric mucosal defensive function in rats with LH lesions. The recovery of the reduced PD by TCA was slow and gastric mucosal lesions were easily formed in the LH lesion group. These results suggest that gastric mucosal ischaemia after lesioning of LH immediately results in the disruption of mucosal defensive function before the formation of visible gastric lesions, and predisposes to the formation of gastric mucosal lesions by a delayed increase in acid secretion.     

The role of cyclic adenosine 3',5'-monophosphate in the ovulatory process of the in vitro perfused rabbit ovary

LH alters ovarian steroidogenesis via adenylate cyclase (AC) activation and cAMP production. Although LH also initiates ovarian follicle rupture, evidence is lacking for involvement of cAMP in this process. This work explores the involvement of cAMP in the ovulation of in vitro perfused rabbit ovaries by comparing LH stimulation of ovaries with that of LH plus 3-isobutyl-1-methyl-xanthine (IBMX), (an inhibitor of phosphodiesterase) and of forskolin (a nonreceptor-specific activator of AC). Venous perfusates were analyzed for cAMP, progesterone, 17 beta-estradiol, and testosterone, ovaries were analyzed for cAMP, and ovulations were noted. LH, LH plus IBMX, and forskolin all increased tissue cAMP levels significantly after 0.5 h, the perfusate levels increasing rapidly thereafter reaching plateau levels, while tissue levels returned to control levels after 2.4 h. LH plus IBMX and forskolin significantly increased cAMP release over LH controls, LH plus IBMX increasing and forskolin decreasing the number of ovulations. Forskolin significantly increased progesterone release over LH controls and, although no other significant steroid differences were seen, strong tendencies existed. Although forskolin could induce ovulations and could induce significantly higher release of cAMP than LH, it resulted in a lower ovulation rate than receptor-specific LH. LH plus IBMX also induced significantly higher cAMP release than LH, as did forskolin, and resulted in a higher ovulation rate than both LH and forskolin. These findings suggest, not only that cAMP production alone is sufficient for ovulation, but also that the receptor specificity of the cAMP production is important for the number of ovulations. Since tissue levels of cAMP peak several hours before ovulation, the cAMP is probably inducing a metabolic pathway leading to ovulation.     

Changes in the pulsatile pattern of luteinizing hormone secretion during the rat estrous cycle

To ascertain whether changes in the pattern of GnRH release from the hypothalmus occur during the 4-day rat estrous cycle, the pattern of LH release was characterized on each day of the estrous cycle, and the results were interpreted in light of the changes in pituitary responsiveness to GnRH previously described by this laboratory to occur during this time. Blood samples were taken from intact, freely moving rats via venous catheters at 6- to 10-min intervals for 3-4 h. LH pulse height and LH interpulse interval were quantified on each day of the cycle, and the transition on the afternoon of proestrus from tonic LH release to the preovulatory LH surge was detailed. The effects on the pattern of LH release during estrus of small doses of GnRH (0.4 ng) and the continuous infusion of the opioid antagonist naloxone were also examined. Plasma LH concentrations (NIAMDD rat LH-RP-1) were determined with a highly sensitive LH RIA. LH pulses were identified using the PULSAR algorithim. The LH interpulse intervals of 46 +/- 2 min on diestrous-1 day, 49 +/- 4 min on diestrous day 2, and 60 +/- 8 min on proestrus immediately before the LH surge were not significantly different. There were no changes immediately preceding the preovulatory LH surge on the afternoon of proestrus in either the LH interpulse interval or the LH pulse height. Instead, the transition from tonic LH secretion to the preovulatory LH surge was found to occur abruptly. These data suggest that an abrupt increase in GnRH secretion during the afternoon of proestrus initiates the dramatic rise in LH concentrations. The pattern of LH secretion during the day of estrus differed significantly from that on the other days of the cycle in that no LH pulses were observed. However, the administration of small pulses of GnRH elicited physiological elevations in LH release. Furthermore, the continuous infusion of naloxone to estrous rats immediately stimulated a pulsatile pattern of LH secretion, with a LH interpulse of 56 +/- 4 min. These data indicate that the absence of LH pulses during estrus may result from a deficit in GnRH release. Similar modifications in GnRH release during the other days of the cycle were inferred from the observed changes in LH pulse heights. The LH pulse height of 21 +/- 3 ng/ml on diestrous day 2 was significantly less than the LH pulse height of 41 +/- 4 ng/ml on diestrous day 1 or 35 +/- 4 ng/ml on proestrus before the surge.(ABSTRACT TRUNCATED AT 400 WORDS)     

Parallelism in the luteinizing hormone responses to opioid and dopamine antagonists in hyperprolactinemic women with pituitary microadenoma

Endogenous opiate peptides are considered to inhibit LH secretion via a dopaminergic mechanism, and increased opioid inhibition of LH secretion has been found in some hyperprolactinemic women with a pituitary microadenoma. To assess the role of endogenous dopaminergic tone in the opioid regulation of LH secretion in such patients, LH responses to an opioid antagonist (naloxone) and a dopamine antagonist (metoclopramide) were determined in 11 women with a prolactinoma. Neither naloxone nor metoclopramide administration induced any change in serum LH levels in normal women during the early follicular phase. In contrast, 7 of the 11 hyperprolactinemic women responded to both antagonists with a significant increase in LH levels. The parallelism in the LH responses to both antagonists in these hyperprolactinemic patients lends further support to a functional link between opioid and dopamine regulation of LH secretion.     

Immunoreactive LH-like substances in serum of hypophysectomized and prepubertal monkeys: inactive in an in vitro LH bioassay.

Serum LH levels in rhesus monkeys are commonly measured by a radioimmunoassay (RIA) utilizing ovine LH as the radioligand and a novel antiserum to ovine LH. Although meeting most criteria of validity, this RIA cross-reacts with serum from demonstrably hypophysectomized monkeys as well as serum from pre-pubertal monkeys. We have utilized the recently developed rat interstitial cell-testosterone assay (RICT) for measurement of serum LH in rhesus monkeys during various endocrine states and have compared the results with those obtained by RIA. The RICT in vitro bioassay was as sensitive, precise, and accurate as the RIA. Partially purified pituitary monkey LH preparations, varying by as much as 100-fold in purity, had similar potency estimates by both assays. The expected biphasic pattern of serum LH levels during the menstrual cycle as well as the usual increase in serum LH levels after ovariectomy was observed with both assays. In each case, however, basal serum LH levels were overestimated by the RIA and peak serum LH levels were underestimated by the RIA as compared to results obtained by the RICT bioassay. The most striking differences between the two assays were observed with serum from hypophysectomized and prepubertal monkeys. Whereas LH-like activity in such samples was high when measured by the RIA, it was undetectable by the RICT bioassay. The ratios of serum LH (RIA/RICT) varied from greater than 7.2 to greater than 17.4 in such sera. These results demonstrate the serious limitations of the ovine LH RIA for measurement of serum LH in rhesus monkeys. It appears that the RICT bioassay may be a suitable alternative method, especially in circumstances other than the menstrual cycle and after ovariectomy.