Postmenopausal hormone replacement: Effects on autonomic, neuroendocrine, and immune reactivity to brief psychological stressors
Postmenopausal hormone replacement: Effects on autonomic, neuroendocrine, and immune reactivity to brief psychological stressors
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DOI：
10.1097/00006842-199801000-00004
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发表时间：
1998-01-01
影响因子：
3.3
通讯作者：
Glaser, R
中科院分区：
文献类型：
--
作者：
Burleson, MH;Malarkey, WB;Glaser, R
目的：绝经后状态增加了妇女对心理压力的生理反应的某些方面;然而，长期用雌激素和孕激素替代对这些反应的影响尚不清楚。我们研究了长期雌激素替代疗法（ERT），无论是否使用孕激素，对短暂实验室应激的生理反应的可能影响。方法：我们研究了三组绝经后妇女：16只服用雌激素，14只服用雌激素和孕激素，25只对照组没有接受替代治疗。心血管，神经内分泌和免疫数据收集在基线和语音和数学任务后。结果如下：在所有组中，应激源降低迷走神经心脏控制（指数为呼吸性窦性心律失常）;增加心率和血浆肾上腺素，促肾上腺皮质激素和皮质醇水平;和改变T淋巴细胞反应（丝裂原诱导的细胞增殖）。自然杀伤细胞溶解和循环白细胞亚群。与对照组相比，任何一种ERT治疗的女性在整个测量期内的总皮质醇水平均较高（反映了雌激素对皮质醇结合球蛋白的影响），且有丝分裂原诱导的胚细胞生成更大。他们还表现出更大的迷走神经退缩和减少有丝分裂原刺激的胚细胞发生的应激反应。联合雌激素和孕激素与较高的肾上腺素和较低的循环总淋巴细胞，T细胞，和CD 4 + T细胞在整个测量期间，和中间水平的迷走神经退缩反应的压力。结论：长期ERT与增强的副交感神经对压力的反应性相关，这表明可能减少对潜在有害的交感神经激活的需求;并且与较高的总体水平和较小的压力诱导的有丝分裂原刺激的胚细胞生成减少相关，这表明上调的T细胞功能。
Objective: Postmenopausal status increases some aspects of women's physiological responses to psychological stress; however, the influences of chronic hormone replacement with estrogen and progestogen on these responses are not known. We investigated possible effects of long-term estrogen replacement therapy (ERT), both with and without progestogen, on physiological reactivity to brief laboratory stressors. Method: We studied three groups of postmenopausal women: 16 on estrogen alone, 14 on estrogen and progestogen, and 25 control participants receiving no replacement therapy. Cardiovascular, neuroendocrine, and immune data were collected at baseline and after speech and math tasks. Results: In all groups, the stressors reduced vagal cardiac control (indexed by respiratory sinus arrhythmia); increased heart rate and plasma epinephrine, adrenocorticotropic hormone, and cortisol levels; and altered T lymphocyte response (measured by mitogen-induced cell proliferation). natural killer cell lysis, and circulating leukocyte subsets. Women on either type of ERT had higher total cortisol levels (reflecting an estro en effect on cortisol binding globulin) and greater mitogen-induced blastogenesis across measurement periods than controls. They also showed greater vagal withdrawal and less decline in mitogen-stimulated blastogenesis in response to the stressors. Combined estrogen and progestogen was associated with higher epinephrine and lower circulating total lymphocytes, T cells, and CD4+ T cells across measurement periods, and with intermediate levels of vagal withdrawal in response to the stressors. Conclusions: Long-term ERT was associated with enhanced parasympathetic responsiveness to stress, suggesting possible reduced demand for potentially detrimental sympathetic activation; and with higher overall levels and smaller stress-induced reductions of mitogen-stimulated blastogenesis, suggesting up-regulated T cell function.