Schurz B, Egarter C, Huber J, Wimmer-Greinecker G, Weindlmayer-Goettl M, Metka M
1. Universitäts-Frauenklinik, Wien.
Zentralbl Gynakol. 1988;110(22):1428-32.
Hot flushes are not caused by a hypergonadotrophinemia. Peaks of gonadotrophin in the serum do not coincide with the cutaneously measured hot flushes. There is an occurrence of hot flushes in hypophysectomized women as well. GnRH and other neurotransmitters (beta-endorphin?) effect the thermoregulation. -
During the climacteric period changes of neurotransmitters, a decrease of catecholestrogens, a decrease of alpha-2-adrenoceptor activity and the ceasing of the ovarian steroid production lead to changes of the endogenous opiate activity and thus to disturbances of the thermoregulation resulting in the occurrence of hot flushes. Low beta-endorphin levels in the peripheral plasma, which increase again after a treatment with estrogens, are found during the climacteric period. On the other hand women with severe hot flushes as an expression of a stress event show enormously increased beta-endorphin values, which normalize again after a hormone substitution therapy, effected by still unknown neuroendocrinological feedback mechanisms.
潮热并非由高促性腺激素血症引起。血清中促性腺激素的峰值与经皮肤测量的潮热并不一致。垂体切除的女性也会出现潮热。促性腺激素释放激素和其他神经递质(β-内啡肽?)影响体温调节。
在更年期,神经递质的变化、儿茶酚雌激素的减少、α-2-肾上腺素能受体活性的降低以及卵巢甾体生成的停止导致内源性阿片活性的改变,进而导致体温调节紊乱,引发潮热。在更年期发现外周血浆中β-内啡肽水平较低,雌激素治疗后该水平会再次升高。另一方面,作为应激事件表现的严重潮热的女性,其β-内啡肽值大幅升高,在激素替代治疗后(通过仍未知的神经内分泌反馈机制)又恢复正常。