BIOASSAY OF SERUM LUTEINIZING HORMONE (LH) AND CHORIONIC GONADOTROPIN

1)之前对人类和实验动物的研究 提示性类固醇激素可能调节脑下垂体 分泌具有生物活性的促性腺激素。我们考察了这个角色 在具有生物活性的黄体生成素分泌中， 稳态E_2输注及内源性E_2的反馈作用 自发和外源性GnRH刺激的搏动性生物活性黄体生成素 放手。E_2抑制平均循环生物活性黄体生成素 浓度，从而导致血浆中显著下降 生物/免疫黄体生成素比率。相反，抗雌激素治疗得到加强。 自发生物活性黄体生成素脉冲频率、脉冲幅度和 脉内和脉间生物/免疫黄体生成素比率。低剂量脉冲 注射外源性促性腺激素释放激素也可提高血浆生物/免疫促黄体生成素水平 比率。但是，他莫昔芬减弱了外源激素的作用。 促性腺激素释放激素进一步提高生物/免疫促黄体生成素比率，这表明 内源性黄体生成素的释放已经在黄体生成素中得到了最大程度的丰富 服用抗雌激素药物期间的生物活性。雌二醇的能力 为了调制LH脉冲信号的特定属性以及 它的频率可能会对以下方面产生重大影响 靶组织功能，也反映了直接作用于 雌二醇通过影响细胞促性腺激素功能 处理和/或末端糖基化的一个或多个方面 黄体生成素分子。2)在我们的早期研究中，使用单一的大剂量 GnRH和/或持续GnRH输注的比例无法透露 外源性促性腺激素释放激素对血浆生物/免疫促黄体生成素的促进作用 比率相反，两个连续次极大调度 外源性促性腺激素释放激素脉冲(每小时10微克)确实产生了 在生物活性黄体生成素立即和优先释放中 随之而来的是血浆BIO/免疫LH值的增加。这些 这些发现可以用脑功能分区来解释。 可释放的LH池。3)生物活性黄体生成素的释放动态 健康的老年男性(60-75岁)显示出显著的 脑下垂体生物释放能力的减弱 活性促性腺激素。生物活性黄体生成素的减少 低剂量(10微克)外源可以揭示释放 GnRH，或通过抗雌激素治疗。年轻和年长的健康男性 表现出相似的基础血浆生物活性黄体生成素浓度和 自发的黄体生成素脉冲特性。然而，脑垂体生物活性黄体生成素 在患有任何一种疾病的老年男性中，储备明显减弱 外源性促性腺激素释放激素或抗雌激素，表明健康的老年男性 表现为生物活性黄体生成素的分泌储备受损 放手。

1) Previous studies in human and experimental animals have suggested that sex steroid hormones may modulate the pituitary secretion of biologically active gonadotropin. We examine the role of E2 in biologically active LH secretion, in men subjected to steady state E2 infusion and feedback actions of endogenous E2 on spontaneous and exogenous GnRH stimulated pulsatile bioactive LH release. E2 suppressed mean circulating bioactive LH concentrations, with a consequent significant decline in the plasma bio/immune LH ratio. Conversely, antiestrogen treatment enhanced spontaneous bioactive LH pulse frequency, pulse amplitude, and intrapulse and interpulse bio/immune LH ratios. Low-dose pulsed injections of exogenous GnRH also increased plasma bio/immune LH ratios. However, tamoxifen attenuated the ability of exogenous GnRH to further enhance the bio/immune LH ratio, which suggests that endogenous LH release was already maximally enriched in LH bioactivity during antiestrogen administration. The ability of E2 to modulate specific properties of the LH pulse signal as well as its frequency may have significant implications in relation to target tissue function, and also reflect direct actions of estradiol on gonadotrope function, through influence the cellular processing and/or one or more aspects of terminal glycosylation of LH molecules. 2) In our early studies using a single large bolus of GnRH and/or continuous GnRH infusions were not able to disclose a stimulatory effect of exogenous GnRH on the plasma bio/immune LH ratio. In contrast, a schedule of two consecutive submaximal pulses (10 micrograms one hour apart) of exogenous GnRH did result in an immediate and preferential release of bioactive LH with a consequent increase in the plasma bio/immuno LH ratio. These findings might be explained by functional compartmentalization of releasable LH pools. 3) The dynamics of bioactive LH release in healthy older men (ages 60-75) have revealed significant attenuation of the pituitary's capacity to release biologically active gonadotropic hormone. The diminution of bioactive LH release could be unmasked by low-dose (10 micrograms) exogenous GnRH, or by antiestrogen treatment. Young and older healthy men exhibit similar mean basal plasma bioactive LH concentrations and spontaneous LH pulse properties. However, pituitary bioactive LH reserve is markedly attenuated in older men challenged with either exogenous GnRH or antiestrogen, indicating that healthy aging men manifest an impaired secretory reserve for biologically active LH release.