Kubota T, Kamada S, Tsuzuki H, Tei A, Saito M
Nihon Sanka Fujinka Gakkai Zasshi. 1987 Jul;39(7):1108-14.
The purpose of this study is to investigate the neuroendocrinological control mechanism of prolactin (PRL) acting on the hypothalamo-pituitary axis during early puerperium. The puerperal women consisted of three groups: the breast-feeding group (n = 39), the bromocriptine (BRC)-treated group (5 mg/day, n = 17) and naloxone-treated group (1 mg iv, n = 16). In each group, 10 mg metoclopramide (MCP), 500 micrograms TRH or 400 mg cimetidine was given intravenously. 1) The plasma PRL levels increased significantly after the injection of MCP, TRH and cimetidine. The peak values of delta PRL levels were 447.0 +/- 62.3 ng/ml after MCP, 278.3 +/- 65.1 ng/ml after TRH and 86.5 +/- 27.3 ng/ml after cimetidine. 2) This PRL increase after the injection of MCP and cimetidine was suppressed significantly by pretreatment with BRC. However, the PRL increase after TRH was not suppressed by pretreatment with BRC. 3) Naloxone had no significant effect on PRL response to MCP and TRH, since the plasma PRL levels rose significantly after the injection of MCP and TRH in the naloxone-treated group. These results revealed that there were different mechanisms of PRL release in MCP and TRH. Furthermore, the PRL releasing mechanism was influenced by histamine H2-receptor, but was not influenced by opioid peptide in early puerperium.
本研究旨在探讨产褥早期泌乳素（PRL）作用于下丘脑 - 垂体轴的神经内分泌控制机制。产褥期妇女分为三组：母乳喂养组（n = 39）、溴隐亭（BRC）治疗组（5mg/天，n = 17）和纳洛酮治疗组（静脉注射1mg，n = 16）。每组均静脉注射10mg甲氧氯普胺（MCP）、500μg促甲状腺激素释放激素（TRH）或400mg西咪替丁。1）注射MCP、TRH和西咪替丁后，血浆PRL水平显著升高。注射MCP后PRL增量的峰值为447.0±62.3ng/ml，注射TRH后为278.3±65.1ng/ml，注射西咪替丁后为86.5±27.3ng/ml。2）BRC预处理可显著抑制注射MCP和西咪替丁后PRL的升高。然而，BRC预处理不能抑制注射TRH后PRL的升高。3）纳洛酮对PRL对MCP和TRH的反应无显著影响，因为纳洛酮治疗组注射MCP和TRH后血浆PRL水平显著升高。这些结果表明，MCP和TRH引起PRL释放的机制不同。此外，在产褥早期，PRL释放机制受组胺H2受体影响，但不受阿片肽影响。
