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儿茶酚胺与垂体功能。2. 正常月经周期女性及催乳素分泌型垂体瘤患者在内源性儿茶酚胺合成抑制前后,催乳素对不同剂量多巴胺的反应。

Catecholamines and pituitary function. 2. Prolactin response to different dopamine doses in normal cycling women and patients with prolactin-secreting pituitary tumors, both before and after endogenous catecholamine synthesis inhibition.

作者信息

Nicoletti I, Filipponi P, Fedeli L, Gregorini G, Ambrosi F, Sfrappini M, Santeusanio F, Brunetti P

出版信息

Horm Metab Res. 1984 Dec;16(12):658-62. doi: 10.1055/s-2007-1014876.

Abstract

The inhibitory effect of various doses of dopamine on serum PRL levels was assessed in both normal cycling women and patients with tumoral hyperprolactinemia before and after endogenous catecholamine synthesis inhibition by alpha-methyl-p-tyrosine, a strong and specific tyrosine-hydroxylase inhibitor. Dopamine infusion induced a significant decrease in the serum PRL levels in both normal cycling and hyperprolactinemic subjects. The mean percent inhibition of baseline PRL induced by the various dopamine infusion rates (0.1, 0.5, 1.0 and 2.0 micrograms/kg/min) was similar in regularly cycling women and in patients with tumoral hyperprolactinemia both before and after endogenous catecholamine synthesis inhibition by alpha-methyl-p-tyrosine. Alpha-methyl-p-tyrosine pretreatment significantly increased serum PRL concentrations in normal women and enhanced their responsiveness to the exogenously administered dopamine. Hyperprolactinemic patients, on the contrary, did not show any significant variation in either basal PRL release or the PRL sensitivity to dopamine infusion after endogenous catecholamine synthesis inhibition. These data indicate that reduced dopamine delivery to the adenomatous lactotroph, either due to a primary hypothalamic abnormality or to a deranged vascular pituitary arrangement, rather than a reduced PRL sensitivity to dopamine inhibition, is the main event accounting for PRL hypersecretion in women with PRL-secreting pituitary tumors.

摘要

在正常月经周期女性及肿瘤性高泌乳素血症患者中,通过α-甲基-对-酪氨酸(一种强效且特异性的酪氨酸羟化酶抑制剂)抑制内源性儿茶酚胺合成前后,评估了不同剂量多巴胺对血清泌乳素(PRL)水平的抑制作用。多巴胺输注使正常月经周期及高泌乳素血症受试者的血清PRL水平均显著降低。在α-甲基-对-酪氨酸抑制内源性儿茶酚胺合成前后,不同多巴胺输注速率(0.1、0.5、1.0和2.0微克/千克/分钟)诱导的基线PRL平均抑制百分比在规律月经周期女性和肿瘤性高泌乳素血症患者中相似。α-甲基-对-酪氨酸预处理显著增加了正常女性的血清PRL浓度,并增强了她们对外源性多巴胺的反应性。相反,高泌乳素血症患者在内源性儿茶酚胺合成抑制后,基础PRL释放或PRL对多巴胺输注的敏感性均未显示出任何显著变化。这些数据表明,无论是由于原发性下丘脑异常还是垂体血管排列紊乱,导致多巴胺向腺瘤性泌乳细胞的输送减少,而非PRL对多巴胺抑制的敏感性降低,是导致分泌PRL的垂体瘤女性PRL分泌过多的主要原因。

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