Csapo A I, Currie W B, Erdos T, Resch B A
Am J Obstet Gynecol. 1978 Oct 15;132(4):464-70. doi: 10.1016/0002-9378(78)90785-8.
Treatment of pregnant rats with antiestradiol (A-E2) serum twice a day, starting at 2100 hours on day 19, sharply increased circulating total estradiol (E2) above control values and drastically reduced the biologically active E2 unbound (E2U) to A-E2 in plasma and uterine tissue. This A-E2-induced and--sustained E2U deficiency was not accompanied by similar changes in plasma and tissue progesterone (P), since P decreased similarly in the control and A-E2--treated rats in preparation for parturition. However, in the A-E2 rats the reduction in E2U was accompanied by a small, though significant, decrease in uterine vein prostaglandin F (PGF) during labor. This A-E2--provoked regulatory imbalance significantly altered normal parturition. In comparison with controls, labor in the A-E2 rats was delayed and prolonged by extended intervals between deliveries of individual fetuses of the same litter. The delay in the onset of labor significantly increased the birth weights of the newborn rats. Whether E2U deficiency is directly responsible for the asynchronic myometrial activity that delays and prolongs labor or whether it is mediated by reduced PGF release remains to be determined.
从第19天21:00开始，每天用抗雌二醇（A-E2）血清对妊娠大鼠进行两次处理，显著提高了循环中总雌二醇（E2）水平，使其高于对照值，并大幅降低了血浆和子宫组织中与A-E2结合的生物活性游离E2（E2U）。这种由A-E2诱导并持续的E2U缺乏，并未伴随着血浆和组织孕酮（P）的类似变化，因为在为分娩做准备的过程中，对照大鼠和接受A-E2处理的大鼠体内P的下降情况相似。然而，在A-E2处理的大鼠中，E2U的减少伴随着分娩时子宫静脉前列腺素F（PGF）的轻微但显著下降。这种由A-E2引发的调节失衡显著改变了正常分娩。与对照相比，A-E2处理的大鼠分娩延迟，同一窝中单个胎儿分娩之间的间隔延长，产程延长。分娩开始的延迟显著增加了新生大鼠的出生体重。E2U缺乏是直接导致延迟和延长产程的子宫肌层活动不同步的原因，还是由PGF释放减少介导，仍有待确定。
