Bjøro K, Stokke K T, Stray-Pedersen S
Scand J Clin Lab Invest Suppl. 1986;184:91-6.
The production rate of four prostanoids (PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2) in human umbilical cords from normal pregnancies (control) and cases with pregnancy-induced hypertension (PIH) were compared. The cords in the PIH-group produced significantly less 6-keto-PGF1 alpha and more TXB2 than did those in the control-group. Production rates of PGE2 and PGF2 alpha were almost equal in the two groups. After stimulation with angiotensin II the PIH-cords displayed a far smaller increase in 6-keto-PGF1 alpha production compared to the control cords. The responses in PGE2 and PGF2 alpha production were again equal in the two groups. The present results indicate that the angiotensin-prostanoid interactions are disturbed in fetal as well as in maternal vessels. Such a disturbance may explain the observed relative hypersensitivity to angiotensin II observed in gravidae prone to develop pregnancy-induced hypertension.
比较了正常妊娠（对照组）和妊娠高血压综合征（PIH）患者的人脐带中四种前列腺素（PGE2、PGF2α、6-酮-PGF1α和TXB2）的生成率。PIH组的脐带生成的6-酮-PGF1α明显少于对照组，而TXB2则多于对照组。两组中PGE2和PGF2α的生成率几乎相等。用血管紧张素II刺激后，与对照脐带相比，PIH脐带中6-酮-PGF1α生成的增加要小得多。两组中PGE2和PGF2α生成的反应再次相等。目前的结果表明，血管紧张素-前列腺素的相互作用在胎儿和母体血管中均受到干扰。这种干扰可能解释了在易患妊娠高血压综合征的孕妇中观察到的对血管紧张素II相对超敏反应。
