Novy M J, Walsh S W
Am J Obstet Gynecol. 1983 Apr 15;145(8):920-31. doi: 10.1016/0002-9378(83)90841-4.
To determine the effects of suppressing fetal and maternal adrenal activity on parturition, we treated pregnant rhesus macaques with dexamethasone (0.25 to 4.0 mg, twice a day) from gestation day 130 until delivery (term = 167 days). Long-term dexamethasone treatment increased gestation length: 71% of fetuses were born postmaturely (after day 175 of gestation; X2 = 52.6; P less than 0.001). The dexamethasone decreased basal levels of maternal estradiol and cortisol, but not progesterone, and abolished the prepartum estrogen and prolactin surges; doses greater than 0.16 mg/kg per day resulted in fetal death but not premature delivery. That vaginal delivery was induced by estradiol benzoate in monkeys with prolonged pregnancy and dead fetuses, but not in those with live fetuses, suggests active fetal inhibition of prostaglandin synthesis. The dexamethasone retarded fetal growth (410 +/- 16 gm versus 501 +/- 5 gm for controls; P less than 0.001) and decreased thymus, spleen, and adrenal weights (P less than 0.01). A less significant decrease in brain weight was noted (P less than 0.1), as were decreases in biparietal diameter, occipitofrontal diameter, and head circumference (P less than 0.05). These results indicate that corticosteroids do not induce premature labor in primates. On the contrary, long-term dexamethasone administration is associated with prolonged pregnancy and suppression of estrogen biosynthesis.
为了确定抑制胎儿和母体肾上腺活动对分娩的影响,我们从妊娠第130天至分娩(足月为167天),用倍他米松(0.25至4.0毫克,每日两次)治疗怀孕的恒河猴。长期使用倍他米松治疗会延长妊娠期:71%的胎儿为过期产(妊娠175天后;X2 = 52.6;P小于0.001)。倍他米松降低了母体雌二醇和皮质醇的基础水平,但未降低孕酮水平,并消除了产前雌激素和催乳素的激增;每天剂量大于0.16毫克/千克会导致胎儿死亡,但不会导致早产。苯甲酸雌二醇能诱导妊娠延长且胎儿死亡的猴子阴道分娩,但不能诱导胎儿存活的猴子阴道分娩,这表明胎儿对前列腺素合成有积极抑制作用。倍他米松延缓了胎儿生长(对照组为501±5克,实验组为410±16克;P小于0.001),并降低了胸腺、脾脏和肾上腺的重量(P小于0.01)。脑重量有不太显著的下降(P小于0.1),双顶径、枕额径和头围也有下降(P小于0.05)。这些结果表明,皮质类固醇不会在灵长类动物中诱发早产。相反,长期给予倍他米松与妊娠期延长和雌激素生物合成受抑制有关。