Stress and the menstrual cycle: short- and long-term response to a five-day endotoxin challenge during the luteal phase in the rhesus monkey.
Stress and the menstrual cycle: short- and long-term response to a five-day endotoxin challenge during the luteal phase in the rhesus monkey.
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DOI：
10.1210/jcem.84.2.5448
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发表时间：
1999-02
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
在此之前，我们报道了恒河猴在卵泡早期中期的5天炎症样应激会严重刺激下丘脑-垂体-肾上腺轴，并对下丘脑-垂体-性腺轴产生影响，延迟卵泡发生，在一些动物中，在治疗后周期会降低黄体功能。由于压力时的内分泌环境可能会影响对压力的反应，我们现在研究在月经周期的黄体期，在黄体酮占主导地位的时候，对类似压力挑战的急性和长期反应。9只周期正常的猴子，从LH峰值后第4-8天开始，每天2次注射内毒素（脂多糖；LPS， 150微克静脉注射），共5天。每天早上注射LPS后3小时和8小时采集血样，监测急性促性腺激素和皮质醇反应。为了验证周期，每天检查月经，每天采血测定雌二醇和黄体酮。记录了两个对照周期、LPS处理周期和两个处理后周期。内毒素激活肾上腺轴：在第一个早晨注射LPS后第3小时，平均（+/- se）皮质醇分泌显著增加（对照组为74.1 +/- 4.9 μ g/dL, P < 0.05），并在第8小时保持升高。这种反应随着时间的推移逐渐降低：在LPS治疗的第5天，皮质醇水平在第3小时仍显著高于对照组（38.5 +/- 5.0微克/分升；P < 0.05），但在第8小时（LPS治疗的第3-5天）已恢复到对照浓度。LPS处理周期黄体期平均综合孕酮含量显著降低（33.5 +/- 3.3 ng/ml，对照周期为48.9 +/- 3.7和54.0 +/- 4.9 ng/ml, P < 0.05），但黄体期长度保持不变。与黄体期当天的对照水平相比，约三分之一的LH和FSH值比平均对照水平低一个SD。LPS给药对两个治疗后周期没有影响，但在治疗后周期1中，9只猴子中有3只的黄体黄体酮仍有所降低。对照周期和治疗后周期的卵泡期长和排卵前雌二醇峰值无差异。与我们之前的研究相比，研究结果说明了在月经周期的不同阶段对压力的特定反应，并支持了这样一种观点，即适度的短期炎症样压力发作有可能微妙地改变月经周期的关键方面。
Previously, we reported that in the rhesus monkey a 5-day inflammatory-like stress during the early-mid follicular phase acutely stimulates the hypothalamic-pituitary-adrenal axis and exerts effects on the hypothalamic-pituitary-gonadal axis, delays folliculogenesis and in some animals decreases luteal function in the post-treatment cycle. Because the endocrine environment at the time of the stress may influence the response to the stress, we now investigate the acute and long-term responses to a similar stress challenge during the luteal phase of the menstrual cycle, at a time of progesterone dominance. Nine monkeys with normal cycles were injected with endotoxin (lipopolysaccharide; LPS, 150 microg i.v.) twice a day for 5 days starting on days 4-8 after the LH peak. Blood samples were taken at hour 3 and hour 8 after each morning LPS injection to monitor the acute gonadotropin and cortisol responses. To verify cyclicity, menses were checked every day, and daily blood samples were taken for estradiol and progesterone measurement. Two control cycles, the LPS treatment cycle, and two post-treatment cycles were documented. Endotoxin activated the adrenal axis: mean (+/-SE) cortisol secretion was significantly increased at hour 3 after the first morning LPS injection (74.1 +/- 4.9 vs. 24.1 +/- 1.8 microg/dL in the control; P < 0.05) and remained elevated at hour 8. This response decreased progressively with time: on day 5 of LPS treatment, the cortisol level was still significantly higher than control at hour 3 (38.5 +/- 5.0 microg/dL; P < 0.05) but had returned to the control concentration by hour 8 (days 3-5 of LPS). Mean integrated progesterone through the luteal phase of the LPS treatment cycle was significantly decreased (33.5 +/- 3.3 ng/ml vs. 48.9 +/- 3.7 and 54.0 +/- 4.9 in the two control cycles; P < 0.05), but luteal phase length remained unchanged. When compared with control levels on the same day of the luteal phase, about one third of LH and FSH values were lower than one SD below mean control levels. LPS administration had no effect on the two post-treatment cycles, except that integrated luteal progesterone in 3 out of 9 monkeys was still reduced in post-treatment cycle 1. There were no differences in follicular phase length and preovulatory estradiol peaks between control cycles and post-treatment cycles. When compared with our previous study, the results illustrate specific responses to stress at different phases of the menstrual cycle and support the notion that a moderate short-term inflammatory-like stress episode has the potential to subtly alter critical aspects of cyclicity.