功能障碍的内皮氧化生物合成在健康吸烟者中,内皮依赖血管扩张受损
R S Barua1, J A Ambrose, L J Eales-Reynolds
1Saint Vincent Catholic Medical Centers of New York, The School of Biomedical and Life Sciences, University of Surrey, UK.
Circulation
|October 17, 2001
概括
吸烟会通过降低氧化 (NO) 生产和内皮NO合成酶 (eNOS) 活性来损害血管功能,导致内皮依赖血管扩张 (EDV) 的降低. 这项研究将吸烟与这些血管变化联系起来.
科学领域:
- 心血管研究研究心血管研究
- 内皮细胞功能 内皮细胞功能
- 氧化生物学 氧化生物学
背景情况:
- 吸烟引起的内皮功能障碍和氧化 (NO) 生物合成障碍的机制尚未完全理解.
- 内皮依赖血管扩张 (EDV) 和NO通路对于血管健康至关重要.
研究的目的:
- 为了研究吸烟,EDV和NO生物合成途径之间的联系.
- 为了将体内血管功能与体内NO生产和内皮NO合成酶 (eNOS) 特性相关联.
主要方法:
- 在健康吸烟者和非吸烟者中评估了流媒体EDV.
- 测量了与参与者的血清化的人类脉内皮细胞 (HUVEC) 的基底和刺激的NO产量.
- 在HUVECs中确定了eNOS蛋白表达和活性.
主要成果:
- 与非吸烟者相比,吸烟者表现出明显较低的EDV.
- 吸烟者的血清减少了NO生产和eNOS活性,同时增加了HUVEC中的eNOS表达.
- 在EDV,NO生产,eNOS活动和eNOS表达之间发现了相关性.
结论:
- 吸烟与EDV,NO生成和eNOS活动的减少有关.
- 吸烟者的eNOS蛋白表达增加可能导致NO生物可用性受损.
- 这项研究提供了体内和体外证据,通过NO通路将吸烟与内皮功能障碍联系起来.
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