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 …

目的 探讨脐静血管舒缩反应及其病理生理学意义与局部一氧化氮合酶变化在妊高征发病中的作用。方法 测定、１４例妊高患者和１４妊娠分娩的 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,计算反应的最大值和亲和力指数值;同时测定脐血管组织ＮＯＳ活性和历乐中一氧化氮代谢产物亚硝基／硝酸基（ＮＯ２／ＮＯ３）浓度。结果（１）对照组脐静脉乙酰胆碱舒张反应曲一的Ｅｍａｘ为（

A study on the role of contractile and relaxant reaction of umbilical vein in vitro and local changes of nitrix oxide synthase in the pathogenesis of pregnancy induced hypertension

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 (NO2-/NO3-) were examined. RESULTS: (1) Relaxtant of the Emax of umbilical vein in the control group in response to acetylcholine was (85.0 +/- 15.0)%, pD2 volume was 4.4 +/- 0.5; However, the Emax (70.0 +/- 13.0)% and the pD2 (3.7 +/- 0.6) were significantly lower in the PIH group (P < 0.01). No significant differences of Emax and pD2 were obtained in phenylephrine-induced vessel contraction and isoprenaline-induced relaxation between the groups (P > 0.05). (2) NOS activity of umbilicahich was significantly lower than that from the control group [(0.5 +/- 0.2) nmol.g-1.min-1] (P < 0.01). The plasma NO2-/NO3- concentration was (38.0 +/- 10.0) mumol/L in the PIH group, which was also lower than that in the control group [(56.0 +/- 14.0) mumol/L] (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.