Levine J D, Taiwo Y O
Department of Medicine, University of California, San Francisco 94143.
Brain Res. 1989 May 15;487(1):143-7. doi: 10.1016/0006-8993(89)90949-9.
The physiological basis of the pain and hyperalgesia observed in patients with Raynaud's phenomenon (RP) is unknown. Since estrogen-induced effects on sympathetic postganglionic neurons (SPGNs) have been implicated in the vasomotor abnormalities in patients with RP, we have studied the effects of estradiol on nociceptive thresholds and noradrenaline sensitivity in a nociceptive flexion reflex in the rat. We report that estradiol induces a catecholamine sensitive hyperalgesia. This hyperalgesia is antagonized by yohimbine (an alpha 2-adrenergic antagonist) but not prazosin (an alpha 1-adrenergic antagonist) as well as by inhibitors of the cyclooxygenase pathway of arachidonic acid metabolism. These data are compatible with the hypothesis that the sensory abnormalities observed in patients with RP may depend on estradiol-induced changes in SPGN, resulting in a sympathetically-dependent production of cyclooxygenase products of arachidonic acid.
雷诺现象（RP）患者出现疼痛和痛觉过敏的生理基础尚不清楚。由于雌激素对交感神经节后神经元（SPGNs）的影响被认为与RP患者的血管运动异常有关，我们研究了雌二醇对大鼠伤害性屈曲反射中伤害性阈值和去甲肾上腺素敏感性的影响。我们报告雌二醇诱导出一种对儿茶酚胺敏感的痛觉过敏。这种痛觉过敏可被育亨宾（一种α2-肾上腺素能拮抗剂）而非哌唑嗪（一种α1-肾上腺素能拮抗剂）以及花生四烯酸代谢的环氧化酶途径抑制剂所拮抗。这些数据与以下假设相符：RP患者中观察到的感觉异常可能取决于雌二醇诱导的SPGN变化，导致花生四烯酸的环氧化酶产物产生交感依赖性。
