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Stress and the Menstrual Cycle: Relevance of Cycle Quality in the Short- and Long-Term Response to a 5-Day Endotoxin Challenge during the Follicular Phase in the Rhesus Monkey 1

1998; Oxford University Press; Volume: 83; Issue: 7 Linguagem: Inglês

10.1210/jcem.83.7.4926

1945-7197

Ennian Xiao, Linna Xia‐Zhang, Alinda Barth, Jun Zhu, Michel Ferin,

Immune Response and Inflammation

The notion that stress activates central and peripheral pathways to inhibit the menstrual cycle is well accepted, but the initial processes through which this occurs have not been investigated.This study uses a relevant nonhuman primate model to document the cyclic endocrine effects imposed by a moderate short-term stress episode in the follicular phase.The stress paradigm is a 5-day inflammatory/immune-like challenge produced by the administration of bacterial endotoxin [lipopolysaccharide (LPS)], which, through the release of endogenous cytokines and other mediators, induces a physiopathological response similar to a bacterial infection.LPS was administered iv twice daily for 5 days starting on days 2-8 of the follicular phase.The stress challenge resulted in a significant lengthening of the follicular phase in all monkeys.Two distinct groups were observed.In group 1 (n ϭ 5), the mean (ϮSE) length of the follicular phase in the LPS-treated cycle was significantly increased, from 10.2 Ϯ 0.2 in control cycle 2 to 30.8 Ϯ 4.3 days (except in one monkey that had a 4-month amenorrheic interval).In group 2 (n ϭ 5), the length of the follicular phase significantly increased but not to exceed the duration of the LPS treatment (9.7 Ϯ 1.1 vs. 13.6 Ϯ 1.2).Estradiol concentrations decreased significantly after LPS in group 1 (34.8Ϯ 5.5 vs. 16.2Ϯ 6.5 pg/mL) and remained suppressed after the challenge.In group 2, estradiol levels remained stationary throughout the 5-day LPS treatment (26.0 Ϯ 6.5 vs. 25.6 Ϯ 3.9).Compared with