ET-1在子痫前期大鼠微血管功能障碍中的作用研究

The role of ET-1 in microvascular dysfunction in rats with preeclampsia

目的探讨内皮素-1(ET-1)在子痫前期微血管功能障碍中的作用。方法健康SD妊娠大鼠16只,随机对数表随机分为模型组和对照组。模型组妊娠期第13天建立减少子宫灌注压(RUPP)子痫前期模型,对照组给予同期行假手术(开关腹)处理。比较两组大鼠妊娠第19天血压、平均子代数目及平均子代体重,检测两组大鼠外周血ET-1表达及肠系膜动脉ET-1介导的血管收缩功能改变。结果模型组大鼠第妊娠19天平均动脉压(120.30±8.50 mmHg)显著高于对照组(81.75±3.37 mmHg);模型组大鼠平均子代数目(9.82±2.14)、平均子代体重(1.53±0.60 g)显著低于对照组(13.09±1.38)、(2.05±1.06 g),以上差异均具有统计学意义(P<0.01)。模型组大鼠外周血ET-1表达水平(40.18±5.64 ng/ml)显著高于对照组(26.72±3.85 ng/ml),模型组大鼠肠系膜动脉ET-1介导的血管最大收缩显著高于对照组,差异具有统计学意义(P<0.05)。结论ET-1表达增加并介导微血管收缩功能增强可能是子痫前期微血管功能障碍的重要作用机制。

Objective To demonstrate the role of endothelin-1(ET-1)in regulating microvascular function in preeclampsia.Methods Sixteen healthy SD pregnancy rats were divided into RUPP group and control group randomly.The RUPP model of preeclampsia was established at 13 days pregnancy,and the control model was treated without RUPP.Blood pressure,fetal survival rate and weight were recorded in two groups at 19 days pregnancy.The ET-1 level in plasma and the contraction in mesenteric artery induced by ET-1 were analysed.Results The average artery blood pressure of RUPP group(120.30±8.50 mmHg)was statistically higher than that of the control group(81.75±3.37 mmHg)at 19 days pregnancy.The counts of survive fetal rats(9.82±2.14)and fetal weight(1.53±0.60 g)were obviously lower than those of the control group with survive fetal rats counts 13.09±1.38 and weight 2.05±1.06 g(P<0.01).The plasma ET-1 level and mesenteric artery contraction induced by ET-1 were dramatically higher in RUPP group comparing with control group(P<0.05).Conclusion Microvascular contraction induced by increasing ET-1 might play an important role in pathogenesis of preeclampsia vascular dysfunction.