Vallet J L, Miles J R, Freking B A
USDA, ARS, U.S. Meat Animal Research Center, P. O. Box 166, State Spur 18D, Clay Center, Nebraska 68933, USA.
Soc Reprod Fertil Suppl. 2009;66:265-79.
Placental insufficiency results in fetal loss, low birth weight, stillbirth, preweaning mortality and poor growth. Placental development begins at conceptus elongation, which is a primary factor controlling the size of the placenta. After elongation, the allantois develops outward from the embryo to establish the allantochorion, which defines the size of the functional placenta. During implantation, chorionic trophoblasts adhere to endometrial epithelial cells. Placental structures known as areolae develop at the openings of the endometrial glands and take up endometrial gland secreted products (histotrophe). Between day 30 and 35 of gestation, the adhered trophoblast-endometrial epithelial bilayer undergoes microscopic folding. Fetal and maternal capillaries develop adjacent to the bilayer and blood flows are arranged in a cross-countercurrent manner. Except for nutrients secreted by the glands, nutrient exchange takes place between these capillaries within these folds. By day 85, the folds deepen and become more complex, increasing surface area. The epithelial bilayer thins and capillaries indent the plane of each layer (but do not penetrate), reducing distance between capillaries. The folded bilayer is surrounded by endometrial stroma on the maternal side and placental stroma on the fetal side. The fetal-placental stroma is partially composed of glycosaminoglycans, the most abundant being hyaluronan and heparan sulfate. Changes in both hyaluronoglucosaminidase and heparanase during placental development suggest that these enzymes play a role in placental development. In addition to structural modifications, various nutrient specific transport mechanisms exist. These mechanisms are likely to be as important to transport of specific nutrients as placental size or structure.
胎盘功能不全可导致胎儿丢失、低出生体重、死产、断奶前死亡率增加及生长发育不良。胎盘发育始于孕体伸长，这是控制胎盘大小的主要因素。伸长后，尿囊从胚胎向外发育形成尿囊绒毛膜，它决定了功能性胎盘的大小。在植入过程中，绒毛膜滋养层细胞粘附于子宫内膜上皮细胞。在子宫内膜腺开口处形成称为乳晕的胎盘结构，并摄取子宫内膜腺分泌的产物（组织营养物质）。在妊娠第30至35天之间，粘附的滋养层-子宫内膜上皮双层结构发生微观折叠。胎儿和母体毛细血管在双层结构附近发育，血流以交叉逆流方式排列。除了腺体分泌的营养物质外，这些褶皱内的毛细血管之间会进行营养物质交换。到第85天时，褶皱加深且变得更加复杂，表面积增加。上皮双层变薄，毛细血管嵌入每一层平面（但不穿透），减少了毛细血管之间的距离。折叠的双层结构在母体一侧被子宫内膜基质包围，在胎儿一侧被胎盘基质包围。胎儿-胎盘基质部分由糖胺聚糖组成，其中最丰富的是透明质酸和硫酸乙酰肝素。胎盘发育过程中透明质酸葡糖胺酶和乙酰肝素酶的变化表明，这些酶在胎盘发育中起作用。除了结构改变外，还存在各种营养物质特异性转运机制。这些机制对于特定营养物质的转运可能与胎盘大小或结构同样重要。
