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皮质醇对排卵前事件产生干扰作用的内分泌基础。

Endocrine basis for disruptive effects of cortisol on preovulatory events.

作者信息

Breen Kellie M, Billings Heather J, Wagenmaker Elizabeth R, Wessinger Emily W, Karsch Fred J

机构信息

Reproductive Sciences Program, University of Michigan, 300 North Ingalls Building, Room 1101 SW, Ann Arbor, Michigan 48109-0404, USA.

出版信息

Endocrinology. 2005 Apr;146(4):2107-15. doi: 10.1210/en.2004-1457. Epub 2004 Dec 29.

DOI:10.1210/en.2004-1457
PMID:15625239
Abstract

Stress activates the hypothalamo-pituitary-adrenal axis leading to enhanced glucocorticoid secretion and concurrently inhibits gonadotropin secretion and disrupts ovarian cyclicity. Here we tested the hypothesis that stress-like concentrations of cortisol interfere with follicular phase endocrine events of the ewe by suppressing pulsatile LH secretion, which is essential for subsequent steps in the preovulatory sequence. Cortisol was infused during the early to midfollicular phase, elevating plasma cortisol concentrations to one third, one half, or the maximal value induced by isolation, a commonly used model of psychosocial stress. All cortisol treatments compromised at least some aspect of reproductive hormone secretion in follicular phase ewes. First, cortisol significantly suppressed LH pulse frequency by as much as 35%, thus attenuating the high frequency LH pulses typical of the preovulatory period. Second, cortisol interfered with timely generation of the follicular phase estradiol rise, either preventing it or delaying the estradiol peak by as much as 20 h. Third, cortisol delayed or blocked the preovulatory LH and FSH surges. Collectively, our findings support the hypothesis that stress-like increments in plasma cortisol interfere with the follicular phase by suppressing the development of high frequency LH pulses, which compromises timely expression of the preovulatory estradiol rise and LH and FSH surges. Moreover, the suppression of LH pulse frequency provides indirect evidence that cortisol acts centrally to suppress pulsatile GnRH secretion in follicular-phase ewes.

摘要

应激会激活下丘脑 - 垂体 - 肾上腺轴,导致糖皮质激素分泌增加,同时抑制促性腺激素分泌并扰乱卵巢周期性。在此,我们检验了这样一个假设:应激样浓度的皮质醇通过抑制促黄体生成素(LH)脉冲式分泌,干扰母羊卵泡期的内分泌事件,而LH脉冲式分泌对排卵前序列的后续步骤至关重要。在卵泡期早期至中期输注皮质醇,将血浆皮质醇浓度提高到隔离诱导值的三分之一、二分之一或最大值,隔离是一种常用的心理社会应激模型。所有皮质醇处理均损害了卵泡期母羊生殖激素分泌的至少某些方面。首先,皮质醇显著抑制LH脉冲频率达35%,从而减弱了排卵前期典型的高频LH脉冲。其次,皮质醇干扰了卵泡期雌二醇升高的适时产生,要么阻止其升高,要么将雌二醇峰值延迟多达20小时。第三,皮质醇延迟或阻断了排卵前LH和促卵泡生成素(FSH)的激增。总体而言,我们的研究结果支持以下假设:血浆皮质醇应激样增加通过抑制高频LH脉冲的发展来干扰卵泡期,这会损害排卵前雌二醇升高以及LH和FSH激增的适时表达。此外,LH脉冲频率的抑制提供了间接证据,表明皮质醇在中枢发挥作用,抑制卵泡期母羊的脉冲式促性腺激素释放激素(GnRH)分泌。

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