Jogee M, Myatt L, Elder M G
Br J Obstet Gynaecol. 1983 Mar;90(3):247-50. doi: 10.1111/j.1471-0528.1983.tb08618.x.
Production of prostacyclin (PGI2) in vitro by human placental cells from pregnancies complicated by fetal growth retardation was significantly reduced compared with that in placental cells from normal pregnancies of either matched gestation or at term. This appeared to be due to a reduction of synthesis of PGI2 rather than to any alteration in the rate of its enzymic metabolism. Addition of oestradiol and progesterone increased PGI2 production by cells from pregnancies with fetal growth retardation in a similar manner to that by cells from first trimester pregnancies, implying that the placental cells are not irreversibly damaged by ischaemia. The decreased PGI2 production by cells of trophoblastic origin may be an aetiological factor in the thrombotic occlusion of the uteroplacental circulation which impairs fetal growth.
与孕周匹配或足月的正常妊娠胎盘细胞相比，患有胎儿生长受限的妊娠中，人胎盘细胞体外产生前列环素（PGI2）的量显著减少。这似乎是由于PGI2合成减少，而非其酶促代谢速率发生任何改变。添加雌二醇和孕酮后，患有胎儿生长受限的妊娠细胞产生PGI2的量增加，其方式与孕早期妊娠细胞相似，这意味着胎盘细胞未因缺血而受到不可逆转的损害。滋养层来源的细胞产生PGI2减少可能是子宫胎盘循环血栓形成阻塞的一个病因，而这种阻塞会损害胎儿生长。
