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出 处:《实用妇产科杂志》2001年第4期204-206,共3页Journal of Practical Obstetrics and Gynecology
摘 要:目的 :通过对比妊高征患者外周及胎盘部位子宫静脉血中一氧化氮 (Nitric Oxide,NO)及内皮素(Endothelin,ET)的浓度 ,了解妊高征时血中血管活性物质浓度发生改变是否与胎盘血管的病变有关。方法 :分别于剖宫产手术前及手术中抽取外周静脉血和胎盘部位子宫静脉血 ,应用硝酸根还原酶与 Griess反应相结合的方法测定 NO;应用放射免疫分析法测定 ET。结果 :妊高征组外周血清 NO2 - / NO3-为 6 5 .5 2± 14.88μmol/ L,胎盘部位子宫静脉血中NO2 - / NO3-为 70 .2 6± 12 .6 0 μmol/ L,二者之间无显著差异。妊高征组外周血浆 ET水平为 5 3.72± 15 .2 8ng/ L,胎盘部位子宫静脉血浆 ET水平为 5 2 .80± 14.19ng/ L ,两者之间无显著性差异 (P>0 .0 5 )。类似结果亦见于正常晚孕组。与正常晚孕组比较 ,妊高征组血中 ET、NO2 - / NO3-水平均显著增高 (P<0 .0 1)。结论 :1妊高征患者外周血中 ET、NO水平高于正常孕妇 ,但与本身胎盘血循环 ET、NO的升高无关。 2妊高征患者的子宫、胎盘血管系统的功能亦遭到破坏。Objectives:To identify the role of placenta in the alterations of Endothelin and Nitric Oxide in patients with preeclampsia by measuring and comparing levels of Endothelin and Nitric Oxide in peripheral circulation and uterine vein at the site of implantation.Methods:15 preeclamptic women were enrolled in this study.Peripheral venous blood samples were collected from all the cases at the beginning of Cesarean section and uterine vein blood samples were taken from the uterine vein draining the placenta before uteruses were incised.Serum NO 2 -/NO 3 -,the end products of NO,were measured with Gricess reaction with nitrate reduclase.Plasma ET were measured by radioimmunoassay.Results:the mean NO 2 -/NO 3 - in peripheral circulation and uterine placenta circulation were 65.52±14.88 μmol/L and 70.26±12.60 μmol/L respectively in preeclampsia.The mean endothelin in peripheral circulation were 53.72±15.28 ng/L,and 52.80 ±14.19ng/L in fetal placental circulation in peeclamptic group.Statistic differences of ET or NO between in systemic and fetal placental circulation were not found in two groups( P >0.05) while patients with preeclampsia had higher concentrations of ET and NO compared with those of normotensive patients( P <0.01).Conclusions:The function of vascular system of fetal placenta is also damaged,which can be demonstrated by the increased ET and NO in fetal placental circulation,but the increase of ET and NO in systemic circulation in preeclampsia is not caused by that in fetal placental circulation.
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