Bronson R, Hamada Y
Fertil Steril. 1978 Sep;30(3):354-61. doi: 10.1016/s0015-0282(16)43525-9.
The uterine content of prostaglandins (PGs) increases following insertion of an intrauterine device (IUD). Such IUD-bearing uteri also exhibit impaired decidualization. Although prostaglandins have been shown to be luteolytic in several species, it is not clear that inhibition of decidualization is mediated solely through alterations in ovarian steroidogenesis. In these experiments, ovariectomized, hormone-replaced pregnant mice, as well as intact mice, were treated systemically with either PGE2 or PGF2alpha so that the extraovarian actions of prostaglandins upon decidualization could be segregated from effects mediated by alterations in ovarian steroidogenesis. The results suggest that the effect of PGF2alpha upon decidualization was mediated via an alteration in ovarian steroidogenesis, but that PGE2 acted independently of the ovary. The hypothesis is presented that alterations in the ratio of E to F prostaglandins elicited within the endometrium by an IUD inhibit decidualization at the uterine level, and that this effect might be mediated by impairment of histamine release from endometrial mast cells.
宫内节育器（IUD）置入后，子宫内前列腺素（PGs）含量会增加。带有IUD的子宫也表现出蜕膜化受损。尽管在几个物种中已证明前列腺素具有溶黄体作用，但尚不清楚蜕膜化的抑制是否仅通过卵巢类固醇生成的改变来介导。在这些实验中，对去卵巢、激素替代的妊娠小鼠以及完整小鼠全身给予PGE2或PGF2α，以便将前列腺素对蜕膜化的卵巢外作用与卵巢类固醇生成改变所介导的作用区分开来。结果表明，PGF2α对蜕膜化的作用是通过卵巢类固醇生成的改变介导的，但PGE2的作用独立于卵巢。提出的假设是，IUD在内膜中引发的E型与F型前列腺素比例的改变在子宫水平抑制蜕膜化，并且这种作用可能是由子宫内膜肥大细胞组胺释放受损介导的。
