Csapo A I, Resch B A
Am J Obstet Gynecol. 1979 Aug 1;134(7):823-7. doi: 10.1016/0002-9378(79)90954-2.
The validity of a new concept, predicting that preterm labor can be induced without oxytocic stimulation by a regulatory imbalance, generated by antiprogesterone (A-P)-provoked P withdrawal (Pw), has been examined in the rat model. At day 19 of pregnancy a single oral dose of the steroidal A-O isoxazol, which inhibits P synthesis, significantly reduced uterine P levels, increased uterine estradiol and prostaglandin F levels, and induced preterm labor. This precocious regulatory imbalance and preterm labor were prevented, by blocking the A-P-induced Pw with P treatment. The regulatory imbalance which triggered the onset of spontaneous labor in the control animals was similar, but it occurred at term rather than before term. The potential of this method in improving the management of medically indicated induction of preterm labor is discussed.
一种新的概念预测,抗孕激素(A-P)引发的孕酮撤退(Pw)所产生的调节失衡可在无催产素刺激的情况下诱发早产,该概念的有效性已在大鼠模型中得到检验。在妊娠第19天,单次口服抑制孕酮合成的甾体类A-O异恶唑,可显著降低子宫孕酮水平,增加子宫雌二醇和前列腺素F水平,并诱发早产。通过用孕酮治疗阻断A-P诱导的Pw,可预防这种早熟的调节失衡和早产。对照动物中引发自然分娩开始的调节失衡与之相似,但发生在足月而非早产之前。文中讨论了该方法在改善医学指征性早产引产管理方面的潜力。