氧化应激在内皮功能障碍中的作用,这种功能障碍是由人类实验性超同囊贫血引起的
P M Kanani1, C A Sinkey, R L Browning
1Departments of Pediatrics, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA.
由氨酸诱导的高水平的同类氨酸,在健康个体中迅速损害血管功能. 这种与氧化应激增加相关的内皮功能障碍可能导致动脉样硬化和高血压.
科学领域:
- 心血管科学 心血管科学
- 血管生物学 血管生物学
- 人体生理学 人体生理学
背景情况:
- 血homocysteine中度升高与动脉样硬化和高血压有关.
- 这项研究调查了同类氨酸是否影响内皮功能和氧化应激.
研究的目的:
- 为了确定是否实验性地增加同类半氨酸水平会导致阻力和导管血管的内皮功能障碍.
- 探索氧化应激在同类氨酸诱导的内皮功能障碍中的作用.
主要方法:
- 健康的受试者接受了L-甲氨酸以诱导高同胞蛋白血症.
- 通过前臂血管扩张到乙胆和流量介导的臂动脉扩张来评估内皮功能.
- 评估了 Askorbic 酸 (抗氧化剂) 对内皮功能的影响.
主要成果:
- 甲因显著损害了前臂阻力血管扩张到乙胆的功能.
- 导管血管内皮功能,通过流介导扩张测量,也显著受损.
- 阿斯科布酸的使用防止了美因引起的内皮功能障碍.
结论:
- 在人体中,实验性升高的homocysteine迅速损害了内皮功能,无论是抵抗和导管血管.
- 这种功能障碍可能解释了同等氨酸,动脉样硬化和高血压之间的关联.
- 增加的氧化应激与homocysteine的不良内皮作用有关.
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