Svedas Eimantas, Nisell Henry, Vanwijk Marja J, Nikas Yorgos, Kublickiene Karolina R
Section for Obstetrics and Gynecology, Department of Clinical Science, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
Am J Obstet Gynecol. 2002 Dec;187(6):1608-16. doi: 10.1067/mob.2002.127378.
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.
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 microscopy.
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.
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.
本研究旨在评估与17β - 雌二醇孵育3小时是否会增强子痫前期女性子宫肌层阻力动脉中血流和缓激肽介导的血管舒张作用，并改变压力诱导的基础张力，同时评估一氧化氮在观察到的反应中的作用。
采用压力肌动描记术，在分离的子宫肌层动脉中，比较与17β - 雌二醇（10⁻⁸mol/L）孵育3小时前后血流和缓激肽介导的血管舒张作用以及对60和80 mmHg腔内压力的反应。在单独的实验中，在一氧化氮合酶抑制剂（10⁻⁴mol/L）存在的情况下，评估一氧化氮对17β - 雌二醇诱导反应的作用。通过扫描电子显微镜评估内皮形态状况。
与子痫前期女性动脉的初始血流介导反应相比，与17β - 雌二醇孵育显著改善了血流介导的血管舒张作用。这种作用是由一氧化氮介导的，因为一氧化氮合酶抑制剂消除了该反应。与正常孕妇动脉相比，子痫前期女性动脉的缓激肽介导的血管舒张作用受损。17β - 雌二醇对子痫前期女性动脉中缓激肽介导的血管舒张作用无影响。与子痫前期女性动脉中60 mmHg时产生的张力相比，80 mmHg时压力诱导的张力增强，与17β - 雌二醇孵育后该张力降低。这种降低也是由一氧化氮介导的。子痫前期女性动脉中存在内皮功能障碍的形态学迹象。
17β - 雌二醇通过一氧化氮介导的途径改善了子痫前期女性分离的子宫肌层动脉中受损的血流介导的血管舒张作用，并降低了基础张力。
