Figueroa R, Martinez E, Fayngersh R P, Jiang H, Omar H A, Tejani N, Wolin M S
Department of Physiology, New York Medical College, Valhalla 10595, USA.
Am J Obstet Gynecol. 1995 Dec;173(6):1800-6. doi: 10.1016/0002-9378(95)90430-1.
Our objective was to determine whether the observed relaxation to lactate and other agents in placental vessels of normal pregnancies is altered in severe preeclampsia.
Isolated placental arteries and veins from women with severe preeclampsia and uncomplicated term pregnancies were precontracted with prostaglandin F2 alpha under 5% oxygen and 5% carbon dioxide with the balance nitrogen (Po2 35 to 38 torr) and then exposed to lactate (1 to 10 mmol/L, pH 7.4, n = 8 to 15), arachidonic acid (0.01 to 10 mumol/L, n = 6 to 13), nitroglycerin (1 nmol to 1 mumol/L, n = 4 to 12), or forskolin (0.01 to 10 mumol/L, n = 6 to 9). The response to lactate was also examined in placental vessels from appropriate-for-gestational-age preterm deliveries (n = 8) for comparison with a similar group with severe preeclampsia (n = 8). The t test and analysis of variance statistics were used.
Relaxation to lactate was markedly inhibited in both placental arteries and veins of women with severe preeclampsia compared with vessels from uncomplicated term or preterm pregnancies. Responses to the other relaxing agents were not altered in the severely preeclamptic vessels.
In severe preeclampsia absence of lactate-induced dilatation of placental vessels may contribute to the fetal complications associated with impaired blood flow and vasospasm.
我们的目的是确定在重度子痫前期中，正常妊娠胎盘血管中观察到的对乳酸和其他药物的舒张反应是否发生改变。
将重度子痫前期妇女和足月正常妊娠妇女的胎盘动脉和静脉在5%氧气、5%二氧化碳及其余为氮气（氧分压35至38托）的条件下用前列腺素F2α预收缩，然后暴露于乳酸（1至10毫摩尔/升，pH 7.4，n = 8至15）、花生四烯酸（0.01至10微摩尔/升，n = 6至13）、硝酸甘油（1纳摩尔至1微摩尔/升，n = 4至12）或福斯可林（0.01至10微摩尔/升，n = 6至9）。还对适于胎龄的早产胎盘血管（n = 8）对乳酸的反应进行了检测，以便与重度子痫前期的类似组（n = 8）进行比较。采用t检验和方差分析统计方法。
与足月正常妊娠或早产妊娠的血管相比，重度子痫前期妇女的胎盘动脉和静脉对乳酸的舒张反应均明显受到抑制。重度子痫前期血管对其他舒张药物的反应未发生改变。
在重度子痫前期，胎盘血管缺乏乳酸诱导的扩张可能导致与血流受损和血管痉挛相关的胎儿并发症。
