内皮氧化合成酶脱在充血性心力衰竭中的功能后果
Lana J Dixon1, David R Morgan, Sinead M Hughes
1Department of Therapeutics and Pharmacology, Queen's University Belfast, 97 Lisburn Rd, Belfast BT9 7BL, Northern Ireland.
Circulation
|April 1, 2003
概括
血小板内皮氧化合成酶 (eNOS) 脱发生在充血性心力衰竭 (CCF) 中,损害血管扩张并减少氧化 (NO) 生产. 这种功能障碍有助于CCF患者的心血管并发症.
科学领域:
- 心血管研究研究心血管研究
- 生物化学 生物化学
- 生理学 生理学 生理学
背景情况:
- 充血性心力衰竭 (CCF) 与受内皮介导的血管扩张 (EMVD) 的损伤有关.
- 由于与超氧化物 (O2*-) 和内皮氧化合成酶 (eNOS) 分离的相互作用,氧化 (NO) 的生物可用性降低,与CCF有关.
- eNOS解导致O2*-生产而不是NO.
研究的目的:
- 在CCF患者中研究eNOS解的功能后果.
- 为了检查血小板中的O2*-和NO生产,作为一种ex-vivo模型.
- 为了将eNOS解与CCF中血管扩展器反应受损的相关性.
主要方法:
- 使用血小板作为一个分隔式的ex-vivo模型来评估O2*-和NO生产.
- 使用Nomega-Nitro-L-Arginine甲基 (L-NAME) 来评估eNOS活性和O2*-生成.
- 测量了依赖内皮和不依赖内皮的血管扩张反应,使用静脉闭塞复合系统学.
主要成果:
- 在18名CCF患者中,在9名患者中确定了eNOS解,在L-NAME给药时,O2*-产量减少.
- 与eNOS结合组相比,在eNOS不结合的CCF组中,血小板衍生NO的产生明显较低.
- 经过eNOS解的患者表现出显著受损的内皮依赖和独立的血管扩张反应.
结论:
- 这项研究首次证实了人类CCF中血小板eNOS脱的证据.
- 在CCF中的eNOS脱与血小板NO产量减少有关.
- 在CCF患者中血管扩张功能受损与eNOS酶解相关.
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