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黄素化未破裂卵泡综合征的组织学和激素记录

Histologic and hormonal documentation of the luteinized unruptured follicle syndrome.

作者信息

Schenken R S, Werlin L B, Williams R F, Prihoda T J, Hodgen G D

出版信息

Am J Obstet Gynecol. 1986 Apr;154(4):839-47. doi: 10.1016/0002-9378(86)90469-2.

DOI:10.1016/0002-9378(86)90469-2
PMID:3083680
Abstract

Histologic and hormonal documentation of a luteinized unruptured follicle that occurred during a spontaneous menstrual cycle in a rhesus monkey is presented. Frequent (every 2 hours) blood sampling to assess midcycle hormonal dynamics in the monkey with the luteinized unruptured follicle and in five monkeys with an ovulatory stigma revealed significant aberrations in the gonadotropin and steroid hormone profiles associated with a luteinized unruptured follicle. Although the midcycle 17 beta-estradiol surge was normal, the monkey with the luteinized unruptured follicle demonstrated (1) blunted midcycle bioassayable luteinizing hormone, immunoassayable luteinizing hormone, and follicle-stimulating hormone surges; (2) absence of disparity in the bioassayable luteinizing hormone: immunoassayable luteinizing hormone ratio during the gonadotropin surge; (3) absence of progesterone and 17 alpha-hydroxyprogesterone secretion during the gonadotropin surge; and (4) delayed and blunted rise in progesterone and 17 alpha-hydroxyprogesterone after the gonadotropin surge. These findings suggest that an impaired luteinizing hormone surge, perhaps mediated by insufficient midcycle progestin secretion, is one possible cause of the luteinized unruptured follicle syndrome.

摘要

本文呈现了在一只恒河猴自发月经周期中出现的黄素化未破裂卵泡的组织学和激素记录。对患有黄素化未破裂卵泡的猴子以及五只具有排卵迹象的猴子进行频繁(每2小时一次)采血,以评估周期中期的激素动态,结果显示与黄素化未破裂卵泡相关的促性腺激素和甾体激素谱存在显著异常。尽管周期中期17β-雌二醇高峰正常,但患有黄素化未破裂卵泡的猴子表现出:(1)周期中期生物活性促黄体生成素、免疫活性促黄体生成素和促卵泡生成素高峰变钝;(2)促性腺激素高峰期间生物活性促黄体生成素与免疫活性促黄体生成素比值无差异;(3)促性腺激素高峰期间无孕酮和17α-羟孕酮分泌;(4)促性腺激素高峰后孕酮和17α-羟孕酮升高延迟且变钝。这些发现表明,促黄体生成素高峰受损,可能由周期中期孕激素分泌不足介导,是黄素化未破裂卵泡综合征的一个可能原因。

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[Spontaneous endogenous LH increase in the stimulated cycle].[刺激周期中内源性促黄体生成素的自发升高]
Arch Gynecol Obstet. 1989;245(1-4):994-9. doi: 10.1007/BF02417653.