Tropper P J, Goland R S, Wardlaw S L, Fox H E, Frantz A G
Department of Obstetrics and Gynecology, Columbia University College of Physicians and Surgeons, New York.
J Perinat Med. 1987;15(3):221-5. doi: 10.1515/jpme.1987.15.3.221.
Corticotropin releasing factor immunoactivity (CRFi) has been identified in the plasma of women in the second half of gestation. There are several lines of evidence supporting a placental source for this hormone. Regulation of placental CRFi is poorly understood. In this study, the effect of a long-acting glucorticoid on the release of placental CRFi was investigated. Eleven women in the third trimester of pregnancy had plasma samples measured for CRFi, ACTH and cortisol before and after receiving 12 mg betamethasone. There was a significant decrease in ACTH (p less than 0.05) and cortisol levels (p less than 0.01) but no change in CRFi. It is concluded that the secretion of CRFi by the placenta is not inhibited by the administration of betamethasone while maternal levels of cortisol and ACTH are lowered. These results suggest that the acute regulation of placental CRFi is distinct from the regulation of hypothalamic CRF.
促肾上腺皮质激素释放因子免疫活性(CRFi)已在妊娠后半期女性的血浆中被鉴定出来。有几条证据支持这种激素的胎盘来源。胎盘CRFi的调节机制尚不清楚。在本研究中,研究了长效糖皮质激素对胎盘CRFi释放的影响。11名妊娠晚期妇女在接受12毫克倍他米松前后,检测血浆中CRFi、促肾上腺皮质激素(ACTH)和皮质醇水平。ACTH水平(p<0.05)和皮质醇水平(p<0.01)显著下降,但CRFi无变化。结论是,给予倍他米松后,胎盘CRFi的分泌未受抑制,而母体皮质醇和ACTH水平降低。这些结果表明,胎盘CRFi的急性调节与下丘脑促肾上腺皮质激素释放因子(CRF)的调节不同。