Paavola L G, Furth E E, Delgado V, Boyd C O, Jacobs C C, Lei H, Strauss J F
Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Biol Reprod. 1995 Aug;53(2):321-38. doi: 10.1095/biolreprod53.2.321.
Premature rupture of fetal membranes can harm infant and mother. It is unclear whether structural changes predispose these membranes to breaking. We thus assessed rat visceral yolk sac placenta (VYSP) and amnion by light and by transmission electron microscopy on Days 18-21 of gestation. Light microscope sections were stained for connective tissue (extracellular matrix) components: collagen, glycoprotein, and glycosaminoglycans/proteoglycans. Some tissue was incubated with chondroitinase ABC. We observed that fetal membranes became increasingly fragile, rupturing readily on Day 21. On Days 18-20, the two epithelial layers of the capsular VYSP were separated by a well-developed, well-vascularized connective tissue layer that stained intensely for all matrix components studied; on Day 21, the connective tissue layer was thinner, moderately stained, and less vascularized. On Days 18-20, the two cellular layers of the amnion were separated by a narrow, compact connective tissue layer that stained modestly for all matrix components; on Day 21, this area was widened and stained faintly. Transmission electron microscopy showed that collagen fibrils of the amnion were abundant, closely packed, and well organized on Days 18-20, whereas on Day 21 they were few in number, widely spaced, and disorganized. Similar changes were present after incubation with chondroitinase ABC. In addition, amniotic epithelial cells were moribund and delaminating, basal laminae were deteriorating or absent, and few cells were at the outer surface of the amnion. All changes preceded parturition. We conclude that the structural integrity of rat fetal membranes is impaired before birth through the loss of connective tissue components and cells, changes that presumably underlie membrane rupture. Lastly, the similarity of structural changes in rat and human fetal membranes point to the potential usefulness of the rat model.
胎膜早破会对婴儿和母亲造成伤害。目前尚不清楚结构变化是否会使这些胎膜易于破裂。因此,我们在妊娠第18 - 21天通过光学显微镜和透射电子显微镜对大鼠内脏卵黄囊胎盘(VYSP)和羊膜进行了评估。光学显微镜切片用结缔组织(细胞外基质)成分进行染色:胶原蛋白、糖蛋白和糖胺聚糖/蛋白聚糖。一些组织用软骨素酶ABC进行孵育。我们观察到胎膜变得越来越脆弱,在第21天很容易破裂。在第18 - 20天,被膜VYSP的两层上皮细胞被一层发育良好、血管丰富的结缔组织层隔开,该结缔组织层对所有研究的基质成分染色都很深;在第21天,结缔组织层变薄,染色适中,血管化程度降低。在第18 - 20天,羊膜的两层细胞层被一层狭窄、紧密的结缔组织层隔开,该结缔组织层对所有基质成分染色适中;在第21天,这个区域变宽且染色很浅。透射电子显微镜显示,羊膜的胶原纤维在第18 - 20天丰富、紧密排列且排列有序,而在第21天数量很少、间隔很宽且排列紊乱。用软骨素酶ABC孵育后也出现了类似的变化。此外,羊膜上皮细胞濒死且分层,基膜退化或缺失,羊膜外表面的细胞很少。所有这些变化都发生在分娩之前。我们得出结论,大鼠胎膜的结构完整性在出生前因结缔组织成分和细胞的丧失而受损,这些变化可能是胎膜破裂的基础。最后一点,大鼠和人类胎膜结构变化的相似性表明大鼠模型具有潜在的应用价值。