Inadequate luteal function is the initial clinical cyclic defect in a 12-day stress model that includes a psychogenic component in the Rhesus monkey.
Inadequate luteal function is the initial clinical cyclic defect in a 12-day stress model that includes a psychogenic component in the Rhesus monkey.
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DOI：
10.1210/jcem.87.5.8500
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发表时间：
2002-05
期刊：
影响因子：
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通讯作者：
E. Xiao;L. Xia-Zhang;M. Ferin
中科院分区：
文献类型：
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作者：
E. Xiao;L. Xia-Zhang;M. Ferin
作为我们开发非人类灵长类动物模型以前瞻性研究不同类型的压力如何影响月经周期的目标的一部分，我们研究了包含重要心因成分的短期压力挑战是否会诱发周期性功能障碍。该研究是在恒河猴中进行的。压力挑战有几个组成部分，包括对系留系统和同时移动到陌生环境的心理反应，以及对安装和断开系留系统所需的简短外科手术的反应。压力挑战持续 12 天，并在月经周期的卵泡期 (n = 5) 或黄体期 (n = 6) 开始。在应激期结束时，移除系绳系统，并将动物放回其正常的饲养环境中。为了监测周期，在前两个对照周期、实验周期和两个应激后周期中每天测量 FSH、LH、E2 和孕酮，而通过测量皮质醇来监测肾上腺内分泌轴反应。动物在短期应激后仍保持排卵；然而，应激周期黄体期（从LH激增+1日到月经-1日）的综合黄体酮分泌量在卵泡期开始应激时显着下降51.6%，在黄体期开始应激时下降30.9%。较低的综合 LH 水平（黄体 5-13）伴随着黄体酮的降低。在第一个应激后周期中，周期参数仍然异常，例如在前一个卵泡期应激后卵泡期延长或在前一个黄体期应激后黄体功能不足。应激后 4 小时内，皮质醇水平比对照组迅速增加 3 倍。此后水平逐渐下降，但在整个短期压力期间仍显着高于对照组。在压力后的前两周内，它们仍然显着较高。总体而言，数据表明，黄体分泌不足代表了压力对正常月经周期造成损害的第一个临床阶段。有趣的是，这种有限的 12 天压力（其中包括显着的心因性成分）在其施加期间之后继续对月经周期产生有害影响。应激后周期中黄体 LH 综合值显着下降表明这些影响可能与生殖轴神经内分泌部分的持续紊乱有关。
As part of our goal to develop nonhuman primate models to prospectively study how different types of stress may affect the menstrual cycle, we have investigated whether a short-term stress challenge that includes a significant psychogenic component can induce cyclic dysfunction. The study was performed in rhesus monkeys. The stress challenge had several components that included the psychological response to both a tethering system and to a simultaneous move to an unfamiliar environment and the response to the short surgical procedures required to install and disconnect the tethering system. The stress challenge lasted for 12 d and was initiated in the follicular (n = 5) or luteal (n = 6) phase of the menstrual cycle. At the end of the stress period, the tethering system was removed, and the animal was returned to its regular housing. To monitor cyclicity, FSH, LH, E2, and progesterone were measured daily throughout the two preceding control cycles, the experimental cycle, and the two poststress cycles, whereas the adrenal endocrine axis response was monitored by measuring cortisol. Animals remained ovulatory after the short-term stress; however, integrated progesterone secretion in the luteal phase (from the day of LH surge +1 to the day of menstruation -1) of the stress cycle was significantly decreased by 51.6% when the stress was initiated in the follicular phase and by 30.9% when it started in the luteal phase. Lower integrated LH levels (luteal d 5-13) accompanied the decreased progesterone. Cyclic parameters were still abnormal in the first poststress cycle, such as a prolonged follicular phase after a stress in the preceding follicular phase or inadequate luteal function after a stress in the preceding luteal phase. Within 4 h of the stress, there was a rapid 3-fold increase in cortisol levels over controls. Levels decreased progressively thereafter but remained significantly higher than controls during the entire short-term stress period. They were still significantly higher in the first 2 wk after stress. Overall, the data suggest that secretory inadequacy of the corpus luteum represents a first clinical stage in the damage that stress can inflict on the normal menstrual cycle. Of interest is the observation that this limited 12-d stress, which includes a significant psychogenic component, continues to produce detrimental effects on the menstrual cycle past the period during which it is exerted. Significant decreases in integrated luteal LH values in the poststress cycle suggest that these effects may be related to continuing disturbances in the neuroendocrine component of the reproductive axis.