负责内皮功能障碍的机制与正常压力妇女的急性雌激素缺乏有关
A Virdis1, L Ghiadoni, S Pinto
1Department of Internal Medicine, University of Pisa, Udine, Italy.
Circulation
|May 16, 2000
概括
急性雌激素缺乏会通过减少氧化 (NO) 的可用性而导致内皮功能障碍. 这与循环氧化酶活性增加的氧化应激有关,而雌激素替代疗法可以逆转这种情况.
科学领域:
- 心血管生理学心血管生理学
- 内分泌学 在内分泌学.
- 血管生物学 血管生物学
背景情况:
- 内皮功能障碍与急性雌激素缺乏有关.
- L-氨酸-氧化物 (NO) 途径和氧化应激是潜在的机制.
- 研究这些途径对于理解雌激素在血管健康中的作用至关重要.
研究的目的:
- 评估急性雌激素缺乏引起的内皮功能障碍是否涉及L-氨酸-NO通路的改变.
- 确定氧化应激,特别是循环氧化酶依赖性途径在这种功能障碍中的作用.
- 评估雌激素替代疗法 (ERT) 对这些血管机制的影响.
主要方法:
- 在健康的女性和患有乳腺瘤的女性中,用压力计整体图测量了前臂血液流量,以应对乙胆 (依赖内皮质) 和酸 (依赖内皮质) 的反应.
- 使用L-氨酸和N(G) -单甲基-L-氨酸 (L-NMMA) 评估了L-氨酸-NO通路.
- 评估了循环氧基因酶的活性,使用印米他辛和维生素C,在卵巢切除和ERT后重复研究.
主要成果:
- 基础血管扩张是由L-阿尔金因和L-NMMA调节的,不受印米他辛或维生素C的影响.
- 经过卵巢切除术后,L-氨酸和L-NMMA的作用减弱,而印梅他辛和维生素C则强化了乙胆诱导的血管扩张.
- 雌激素替代疗法恢复了L-氨酸和L-NMMA的效果,并取消了因多美或维生素C的强化.
结论:
- 由于急性雌激素缺乏导致的内皮功能障碍是由于氧化 (NO) 可用性降低的结果.
- 循环氧基因酶依赖的氧化应激可能有助于这种NO减少.
- 雌激素替代疗法有效地逆转了这些由雌激素缺乏引起的血管变化.
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