Goland R S, Jozak S, Warren W B, Conwell I M, Stark R I, Tropper P J
Department of Medicine, Columbia University College of Physician and Surgeons, New York, New York 10032.
J Clin Endocrinol Metab. 1993 Nov;77(5):1174-9. doi: 10.1210/jcem.77.5.8077309.
CRH is synthesized in the hypothalamus and released in response to stress into the portal hypophyseal blood; an additional site of synthesis, the placenta, is present only during pregnancy. Placental CRH is released into the maternal and fetal circulation during human pregnancy, and we hypothesized that the chronic fetal stress associated with fetal growth retardation may stimulate placental CRH release. We measured plasma CRH concentrations in the umbilical cord blood of 28 growth-retarded fetuses and 28 normally grown fetuses matched for gestational age and mode of delivery. Plasma ACTH, dehydroepiandrosterone sulfate (DHEAS), and cortisol were also measured in the umbilical cord samples to determine if CRH levels were correlated with levels of pituitary and adrenal hormones. The mean umbilical cord plasma CRH level in the growth-retarded fetuses was 206 +/- 25.8 pmol/L, which was significantly higher than that in the normally grown fetuses matched for gestational age, presence or absence of labor, and mode of delivery (49.4 +/- 16.7 pmol/L; P < 0.01). The mean plasma ACTH level in the growth-retarded fetuses (5.7 +/- 1.2 pmol/L) was significantly higher than that in the normally grown fetuses (3.3 +/- 0.7 pmol/L; P < 0.05). The mean cortisol concentration in the growth-retarded fetuses was 260 +/- 32.5 nmol/L, and that in the normally grown fetuses was 220 +/- 40 nmol/L. The mean DHEAS level was significantly lower in the growth-retarded fetuses (4.8 +/- 0.6 mumol/L) than that in the normally grown fetuses (7.7 +/- 0.6 mumol/L; P < 0.001). There was a significant correlation between umbilical cord plasma CRH and both ACTH and cortisol concentrations as well as a significant negative correlation between CRH and DHEAS levels in the growth-retarded fetuses. The umbilical cord plasma CRH level is extremely elevated in growth-retarded fetuses compared to that in normal fetuses. Placental CRH, like hypothalamic CRH, may be stimulated in conditions of chronic stress and may modulate fetal pituitary-adrenal function in high risk pregnancies.
促肾上腺皮质激素释放激素（CRH）在下丘脑合成，并在应激反应时释放到垂体门脉血中；另一个合成部位是胎盘，但仅在孕期存在。人类孕期胎盘CRH释放到母体和胎儿循环中，我们推测与胎儿生长受限相关的慢性胎儿应激可能刺激胎盘CRH释放。我们测量了28例生长受限胎儿和28例孕龄及分娩方式匹配的正常生长胎儿脐带血中的血浆CRH浓度。还测量了脐带样本中的血浆促肾上腺皮质激素（ACTH）、硫酸脱氢表雄酮（DHEAS）和皮质醇，以确定CRH水平是否与垂体和肾上腺激素水平相关。生长受限胎儿脐带血浆CRH平均水平为206±25.8 pmol/L，显著高于孕龄、有无临产及分娩方式匹配的正常生长胎儿（49.4±16.7 pmol/L；P<0.01）。生长受限胎儿血浆ACTH平均水平（5.7±1.2 pmol/L）显著高于正常生长胎儿（3.3±0.7 pmol/L；P<0.05）。生长受限胎儿皮质醇平均浓度为260±32.5 nmol/L，正常生长胎儿为220±40 nmol/L。生长受限胎儿DHEAS平均水平（4.8±0.6 μmol/L）显著低于正常生长胎儿（7.7±0.6 μmol/L；P<0.001）。生长受限胎儿脐带血浆CRH与ACTH和皮质醇浓度均呈显著正相关，与DHEAS水平呈显著负相关。与正常胎儿相比，生长受限胎儿脐带血浆CRH水平极度升高。胎盘CRH与下丘脑CRH一样，可能在慢性应激状态下受到刺激，并可能在高危妊娠中调节胎儿垂体-肾上腺功能。
