BIOASSAY OF SERUM LUTEINIZING HORMONE (LH) AND CHORIONIC GONADOTROPIN

对LH生物活性和性腺受体的研究提供了以下见解： 人、恒河猴和猕猴垂体-性腺功能调节 大鼠 调节血浆LH的频率和生物免疫比（B：I） 脉冲还提供了一种重要的生理机制， 卵巢和睾丸可获得的有效LH浓度。 的 循环LH的生物活性似乎受到性腺激素的快速调节， 类固醇（即正常男性的B：I高于骑自行车的女性;去势 在大鼠中降低B：I），可能通过糖基化的变化。 还有， 去势动物LH的B：I降低可能与 LH分泌速率增加。 老年男性前列腺癌患者的B：I 发现低，表明B：I变化的潜在重要性， 年龄和疾病。 回归分析显示， B：I和血浆睾酮随年龄增长而降低，40岁以上的男性患者I和血浆睾酮随年龄增长而降低，40岁以上的男性患者I和血浆睾酮随年龄增长而降低，40岁以上的男性患者I和血浆睾酮随年龄增长而降低， B：I. 这些发现表明，LH的定性性质随着年龄的增长而变化。 男性衰老和疾病的功能。 LH分泌的异常性质 低B：I可能与阳痿患者的病因相关， 正常免疫反应性垂体激素和LH周期性， 睾丸激素水平 促性腺激素释放激素或克罗米芬治疗期间B：I升高 在患有这种类型的疾病的患者中，并且已知具有垂体 钙化，表明垂体GnRH之间的功能关系 暴露和分泌LH的更大效力。 内分泌 可逆的内源性雌激素过量对 垂体-性腺轴的详细研究分析了一个 患有产生雌激素的肾上腺肿瘤的患者。 在这种情况下， 性腺功能减退症可归因于生物活性LH的选择性减少和低 B：I比率。 LH的减少可能是由于E2的作用， 下丘脑水平，以减少GnRH分泌，并从直接影响 垂体LH加工 我们还证明了腺嘌呤类似物 （4-氨基吡唑并-（3，4-d）-嘧啶）对GnRN具有抑制作用 从下丘脑释放，并正在分析这种关系， 影响神经激素分泌机制。

Studies on LH bioactivity and gonadal receptors have provided insights into the regulation of pituitary-gonadal function of man, rhesus monkey and rat. Modulation of the frequency and bio:immuno rations (B:I) of plasma LH pulses also provides an important physiological mechanism for regulating the concentrations of effective LH available to the ovary and testis. The bioactivity of circulating LH appears to be rapidly modulated by gonadal steroids (i.e. normal men have higher B:I than cycling females; castration in rats decrease the B:I), possibly via changes in glycosylation. Also, the decrease in B:I of LH in castrated animals could be related to increased LH secretion rate. The B:I in older men with prostatic cancer as found to be low, indicating the potential importance of changes in B:I with age and sickness. Regression analysis showed an inverse relationship of B:I and plasma testosterone with age, and ill men over age 40 had lower B:I. These findings indicate that the qualitative nature of LH varies as a function of aging and illness in men. The abnormal nature of LH secreted with low B:I may be etiologically relevant in patients with impotence and normal immunoreactive pituitary hormones and LH periodicity, and low normal testosterone levels. The increased B:I during GnRH or clomiphene therapy in a patient with this type of disorder, and known to have pituitary calcification, indicated a functional relationship between pituitary GnRH exposure and the greater potency of secreted LH. The endocrine consequences of reversible endogenous estrogen excess on the pituitary-gonadal axis in man were analyzed in a detailed study of a patient with an estrogen-producing adrenal tumor. In this case, hypogondism was attributable to selective reduction in bioactive LH and low B:I ratio. The LH reduction could result from E2 action at the hypothalamic level to reduce GnRH secretion, and from direct effects on pituitary LH processing. We have also demonstrated that the adenine analog (4-Aminopyrazolo-(3,4-d)-Pyrimidine) has an inhibitory action on GnRN release from the hypothalamus, and are analyzing the relation of this effect to the mechanism of neurohormone secretion.