Endothelial dysfunction in uterine circulation in preeclampsia: Can estrogens improve it?
Endothelial dysfunction in uterine circulation in preeclampsia: Can estrogens improve it?
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DOI：
10.1067/mob.2002.127378
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发表时间：
2002-12-01
影响因子：
9.8
通讯作者：
Kublickiene, KR
中科院分区：
文献类型：
--
作者：
Svedas, E;Nisell, H;Kublickiene, KR
目的：本研究的目的是评估与17 β-雌二醇孵育3小时是否会增强血流和缓激肽介导的扩张，并改变先兆子痫妇女子宫肌层阻力动脉中压力诱导的基础张力，并评估一氧化氮在观察到的反应中的作用。在与17 β-雌二醇（10（-8）mol/L）孵育3小时之前和之后，比较血流和缓激肽介导的扩张以及对60和80 mm Hg管腔内压的反应。在离体子宫肌层动脉中应用压力肌造影技术。在单独的实验中，在一氧化氮合酶抑制剂（10（-4）mol/L）的存在下评价了一氧化氮对17 β-雌二醇诱导的反应的作用。内皮细胞的形态条件进行了评估，通过扫描电子显微镜结果：孵育与17 β-雌二醇显着改善血流介导的扩张相比，初始血流介导的反应，动脉先兆子痫的妇女。这种效应是一氧化氮介导的，因为一氧化氮合酶抑制剂消除了这种反应。与正常孕妇的动脉相比，先兆子痫妇女的动脉表现出受损的缓激肽介导的扩张。17 β-雌二醇对先兆子痫妇女的缓激肽介导的动脉扩张没有影响。与先兆子痫妇女动脉中在60 mm Hg下形成的张力相比，在80 mm Hg下增强的压力诱导张力在与17 β-雌二醇孵育后降低。这种减少也是一氧化氮介导的。血管内皮功能障碍的形态学迹象是明显的，在动脉从妇女与先兆子痫。结论：17 β-雌二醇改善受损的血流介导的扩张和降低基础张力通过一氧化氮介导的途径在子宫肌层动脉从妇女与先兆子痫。
OBJECTIVE: The purpose of this study was to evaluate whether a 3-hour incubation with 17beta-estradiol will enhance blood flow- and bradykinin-mediated dilatation and alter pressure-induced basal tone in myometrial resistance arteries from women with preeclampsia and to evaluate the role of nitric oxide in the responses that were observed.STUDY DESIGN: Blood flow- and bradykinin-mediated dilatation and responses to intraluminal pressure of 60 and 80 mm Hg were compared before and after 3 hours of incubation with 17beta-estradiol (10(-8) mol/L) in isolated myometrial arteries with the pressure myography technique. In separate experiments, the role of nitric oxide on 17beta-estradiol-induced responses was evaluated in the presence of the nitric oxide synthase inhibitor (10(-4) mol/L). Endothelial morphologic condition was evaluated by scanning electron microscopyRESULTS: Incubation with 17beta-estradiol significantly improved blood flow-mediated dilatation compared with initial blood flow-mediated response in arteries from women with preeclampsia. This effect was nitric oxide mediated, because the nitric oxide synthase inhibitor abolished the response. Arteries from women with preeclampsia demonstrated impaired bradykinin-mediated dilatation compared with that obtained in arteries from normal pregnant women. The 17beta-estradiol had no effect on bradykinin-mediated dilatation in arteries from women with preeclampsia. The enhanced pressure-induced tone at 80 mm Hg compared with the tone that developed at 60 mm Hg in arteries from women with preeclampsia was reduced after incubation with 17beta-estradiol. This reduction was also nitric oxide mediated. Morphologic signs of endothelial dysfunction were evident in arteries from women with preeclampsia.CONCLUSION: The 17beta-estradiol improved impaired blood flow-mediated dilatation and reduced basal tone through a nitric oxide-mediated pathway in isolated myometrial arteries from women with preeclampsia.