Garfield R E, Gasc J M, Baulieu E E
Department of Neurosciences, McMaster University, Hamilton, Ontario, Canada.
Am J Obstet Gynecol. 1987 Nov;157(5):1281-5. doi: 10.1016/s0002-9378(87)80315-0.
The effects of the antiprogesterone compound RU 486 on preterm delivery, myometrial gap junctions, and plasma levels of steroid hormones were investigated in pregnant rats. Injection of RU 486 on day 16 of gestation resulted in prolonged delivery beginning after 24 hours. The preterm birth initiated by RU 486 was preceded and accompanied by the extensive development of gap junctions between myometrial cells. R 5020, but neither progesterone nor dexamethasone, prevented preterm birth and the development of gap junctions. Estrogen and progesterone levels declined after RU 486 treatment but only after a major proportion of the fetuses were delivered. This study indicates that progesterone may normally inhibit uterine contractility by suppressing the genome responsible for the expression of gap junctions.
在妊娠大鼠中研究了抗孕酮化合物RU 486对早产、子宫肌层缝隙连接和甾体激素血浆水平的影响。在妊娠第16天注射RU 486导致24小时后开始分娩延长。RU 486引发的早产之前和期间子宫肌层细胞间缝隙连接广泛发展。R 5020可预防早产和缝隙连接的发展,而孕酮和地塞米松则不能。RU 486治疗后雌激素和孕酮水平下降,但仅在大部分胎儿娩出后才出现。本研究表明,孕酮通常可能通过抑制负责缝隙连接表达的基因组来抑制子宫收缩力。