脐静脉体外舒缩反应及局部一氧化氮合酶变化在妊高征发病中的作用

A Study on the Role of Contractile and Relaxant Reaction of Umbilical Vein in Vitro and Local Changes of Nitric Oxide Synthase in the Pathogenesis of Pregnancy Induced Hypertension

目的探讨脐静脉血管舒缩反应及其病理生理学意义与局部一氧化氮合酶（ｎｉｔｒｉｃｏｘｉｄｅｓｙｎｔｈａｓｅ，ＮＯＳ）变化在妊高征发病中的作用。方法测定１４例妊高征患者（妊高征组）和１４例正常妊娠妇女（对照组）分娩的新生儿脐静脉在离体血管功能实验中，对苯肾上腺素、异丙肾上腺素和乙酰胆碱的收缩和舒张反应曲线，计算反应的最大值（Ｅｍａｘ）和亲和力指数（ｐＤ２）值；同时测定脐血管组织ＮＯＳ活性和血浆中一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）代谢产物亚硝酸基／硝酸基（ＮＯ－２／ＮＯ－３）浓度。结果⑴对照组脐静脉乙酰胆碱舒张反应曲线的Ｅｍａｘ为（８５．０±１５．０）％，ｐＤ２值为４．４±０．５；而妊高征组脐静脉乙酰胆碱舒张反应曲线明显向右下偏移，其Ｅｍａｘ（７０．０±１３．０）％和ｐＤ２值（３．７±０．６）均低于对照组，差异有极显著性（Ｐ＜０．０１）；两组脐血管对苯肾上腺素的收缩反应曲线和对异丙肾上腺素的舒张反应曲线相对无明显偏移。⑵妊高征组脐静脉组织ＮＯＳ活性为（０．３±０．１）ｎｍｏｌ·ｇ－１·ｍｉｎ－１，对照组为（０．５±０．２）ｎｍｏｌ·ｇ－１·ｍｉｎ－１，两组比较，差异有极显著性（Ｐ＜０．０１）；其血浆中ＮＯ－２?

Objective To study the contractile and relaxant reaction of human umbilical veins in vitro from pregnancy induced hypertension (PIH) patients, pathophysiological significance and the role of local changes of nitric oxide synthase(NOS)in the pathogenesis of PIH. Methods The contractile and relaxant curves of umbilical vein in response to phenylephrine ,isoprenaline and acetylcholine were recorded in the PIH group and normal pregnancy group(control group) .The maximum effect (Emax) and affinity index (pD2) volume were calculated. Meanwhile, the NOS activity in the blood vessel tissue and the plasma concentration of nitric oxide metabolite (NO-2/NO-3) were examined. Results (1) Relaxtant of the Emax of umbilical vein in the control group in response to acetylcholine was (85.015.0)%,pD2 volume was 4.40.5; However,the Emax (70.013.0)% and the pD2 (3.70.6) were significantly lower in the PIH group (P<0.01).No significant differences of Emax and pD2 were obtained in phenylephrineinduced vessel contraction and isoprenalineinduced relaxation between the groups(P>0.05).(2) NOS activity of umbilicahich was significantly lower than that from the control group lg-1min-1] (P<0.01).The plasma NO-2/NO-3 concentration was(38.010.0)mol/L in the PIH group, which was also lower than that in the control group ](P<0.01). Conclusions The abnormal function of endothelium system and abnormal metabolism of nitric oxide in blood vessel, which resulted in the decreased endothelium dependent relaxation, might be possible mechanism involved in the pathogenesis of PIH.