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目的 探讨一氧化氮在妊高征发病中的作用及其与内皮素、雌激素的关系。方法 采用放射免疫法和酶法测定 30例妊高征患者 (妊高征组 )和 30例正常晚期妊娠妇女 (对照组 )产前及产后 72h的血清亚硝酸盐 (NO2 -) ,血清雌激素 (E2 )和血浆内皮素 (ET)的物质的量浓度 ,并对其中 10例重度妊高征及 5例正常妊娠者的胎盘用免疫组织化学进行内皮型一氧化氮合成酶 (eNOS)的定位及半定量研究。结果 1)产前妊高征组NO2 -、ET物质的量浓度明显高于对照组 (P <0 .0 0 1) ;2 )妊高征组产后 72h的NO2 -、ET、E2 物质的量浓度明显低于产前 (P <0 .0 0 1) ;3)妊高征组及对照组产前、产后的NO2 -、EET、E2 物质的量浓度之间均无明显相关性 (P >0 .0 5 ) ;4)妊高征胎盘的eNOS活性明显低于正常者 ,两者分布上亦有差异。结论 妊高征患者血中一氧化氮 (NO)水平较正常孕妇的高 ,过多的NO是由诱导型一氧化氮合成酶 (iNOS)作用生成 ,他加重了血管内皮细胞的损伤 ,引起内皮素 (ET)的合成和释放增加 ,导致血管痉挛 ;雌激素的减少加重了血管痉挛 ,从而发生妊高征
Objective To explore the role of nitric oxide in the pathogenesis of PIH and its relationship with endothelin and estrogen. Methods Serum nitric oxide (NO2 -), serum estradiol (E2) levels in preeclampsia and postpartum 72 h were measured in 30 PIH patients and 30 normal pregnant women (control group) by radioimmunoassay and enzymatic method. (E2) and plasma endothelin (ET). The placenta of 10 cases with severe PIH and 5 normal pregnancy were used for the localization of endothelial nitric oxide synthase (eNOS) by immunohistochemistry And semi-quantitative studies. Results 1) Pretreatment PIH group NO2 -, ET substance concentration was significantly higher than the control group (P <0 01); 2) PIH group postnatal 72h NO2 -, ET, E2 substance (P <0.01). (3) There was no significant correlation between the concentration of NO2 -, EET and E2 in preeclampsia and postnatal pregnancy (P> 0 .0 5). 4) The eNOS activity of placenta in pregnancy-induced hypertension was significantly lower than that in normal subjects. Conclusions The level of nitric oxide (NO) in patients with PIH is higher than that in normal pregnant women. Excess NO is produced by inducible nitric oxide synthase (iNOS), which aggravates the damage of vascular endothelial cells and causes endothelial Increased synthesis and release of the hormone (ET) leads to vasospasm; decreased estrogen exacerbates vasospasm and leads to pregnancy-induced hypertension