Mechanisms responsible for endothelial dysfunction associated with acute estrogen deprivation in normotensive women
Mechanisms responsible for endothelial dysfunction associated with acute estrogen deprivation in normotensive women
复制标题
DOI：
10.1161/01.cir.101.19.2258
复制
发表时间：
2000-05-16
期刊：
影响因子：
37.8
通讯作者：
Salvetti, A
中科院分区：
文献类型：
--
作者：
Virdis, A;Ghiadoni, L;Salvetti, A
本研究的目的是评估急性雌激素剥夺相关的内皮功能障碍是否是由L-精氨酸-一氧化氮（NO）途径和氧化应激的改变引起的。（年龄，45.7 +/- 5.4岁）和18名患有平滑肌瘤的生育妇女（年龄，44.5 ± 5.1岁），我们研究了前臂血流（应变式体积描记法）由臂内乙酰胆碱引起的变化（0.15、0.45、1.5、4.5或15 μ g·100 mL（-1）·min（-1））或硝普钠（1、2或4 μ g·100 mL（-1）·min（-1）），分别为内皮依赖性或非依赖性血管扩张剂。NO通路通过在L-精氨酸作用期间重复乙酰胆碱来评估。（200 μ g·100 mL（-1）·min（-1）; 13名对照受试者和9名患者）或N-G-单甲基-L-精氨酸（L-NMMA; 100 μ g·100 mL（-1）·min（-1）; 13名对照受试者和9名患者）;环氧化酶衍生的血管收缩剂的产生通过重复乙酰胆碱来评估，（50 μ g·100 mL（-1）·min（-1）：13名对照受试者和9名患者）或维生素C（8 mg·100 mL（-1）·min（-1）; 13名对照受试者和9名患者）。患者在卵巢切除术后1个月内重复研究，并在雌激素替代治疗（ERT; 17 β-雌二醇TTS，50 μ g/d）3个月后再次重复研究。在基础上，L-精氨酸和L-NMMA分别增强和抑制乙酰胆碱的血管舒张作用（P
Background-The goal of this study was to evaluate whether endothelial dysfunction associated with acute estrogen deprivation is caused by an alteration in the L-arginine-nitric oxide (NO) pathway and oxidative stress.Methods and Results-In 26 healthy women (age, 45.7 +/- 5.4 years) and 18 Fertile women with leiomyoma (age, 44.5 +/- 5.1 years), we studied forearm blood flow (strain-gauge plethysmography) changes induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, or 15 mu g.100 mL(-1).min(-1)) or sodium nitroprusside (1, 2, or 4 mu g.100 mL(-1).min(-1)), an endothelium-dependent or -independent vasodilator, respectively. The NO pathway was evaluated by repeating acetylcholine during L-arginine (200 mu g.100 mL(-1).min(-1); 13 control subjects and 9 patients) or N-G-monomethyl-L- arginine (L-NMMA; 100 mu g.100 mL(-1).min(-1); 13 control subjects and 9 patients); production of cyclooxygenase-derived vasoconstrictors was assessed by repeating acetylcholine during indomethacin (50 mu g.100 mL(-1).min(-1): 13 control subjects and 9 patients) or vitamin C (8 mg.100 mL(-1).min(-1); 13 control subjects and 9 patients). Patients repeated the study within I month after ovariectomy and again after 3 months of estrogen replacement therapy (ERT; 17 beta-estradiol TTS, 50 mu g/d). Basally, vasodilation to acetylcholine was potentiated and inhibited by L-arginine and L-NMMA, respectively (P