Kubota T, Nagae M, Kamata S, Oohara M, Saito M, Kumasaka T, Yaoi Y
Nihon Sanka Fujinka Gakkai Zasshi. 1985 Jun;37(6):945-54.
The purpose of this study was to investigate the prolactin (PRL) releasing mechanism of the hypothalamo-pituitary axis during labor and early puerperium. Ten full-term gravidas during labor and 42 women in early puerperium were examined in this study. The plasma PRL levels rose significantly (p less than 0.001 approximately 0.05) after an intravenous bolus of 10mg metoclopramide (MCP). The peak values for PRL increase were 609.3 +/- 194.1ng/ml during labor and 447.0 +/- 62.3ng/ml in early puerperium. However, there were no significant differences in PRL response to MCP between these two groups. The plasma PRL levels dropped significantly (p less than 0.001 approximately 0.01) after an oral administration of 2.5mg bromocriptine (BRC), and the PRL release from the pituitary by MCP was suppressed significantly (p less than 0.001) by pretreatment with BRC in the puerperium. In addition, no significant changes in plasma 17 beta-estradiol (E2), progesterone (P) and cortisol levels could be observed after MCP. We concluded that the control mechanism of PRL secretion remained unchanged during labor and early puerperium.
本研究旨在探讨分娩期及产褥早期下丘脑 - 垂体轴催乳素（PRL）的释放机制。本研究检查了10名分娩期足月孕妇和42名产褥早期妇女。静脉推注10mg甲氧氯普胺（MCP）后，血浆PRL水平显著升高（p小于0.001至0.05）。分娩期PRL升高的峰值为609.3±194.1ng/ml，产褥早期为447.0±62.3ng/ml。然而，两组之间PRL对MCP的反应无显著差异。口服2.5mg溴隐亭（BRC）后，血浆PRL水平显著下降（p小于0.001至0.01），在产褥期，BRC预处理可显著抑制MCP引起的垂体PRL释放（p小于0.001）。此外，MCP后血浆17β-雌二醇（E2）、孕酮（P）和皮质醇水平未观察到显著变化。我们得出结论，分娩期及产褥早期PRL分泌的控制机制保持不变。
