肥胖和睡眠呼吸暂停的血管炎症
Sanja Jelic1, David J Lederer, Tessa Adams
1Columbia University College of Physicians and Surgeons, Division of Pulmonary, Allergy, and Critical Care Medicine, PH8 Center, Room 101, 630 W 168th St, New York, NY 10032, USA. sj366@columbia.edu
Circulation
|February 18, 2010
概括
阻塞性睡眠呼吸暂停 (OSA),而不是肥胖,显著驱动血管内皮功能障碍和炎症. 用持续的正气道压力治疗OSA可以改善内皮功能,减少氧化应激.
科学领域:
- 心血管科学 心血管科学
- 睡眠医学 睡眠医学
- 血管生物学 血管生物学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 在肥胖中很常见,并与心血管疾病风险有关.
- 肥胖和OSA都会导致血管内皮炎症.
- 这项研究旨在区分OSA对内皮的影响与肥胖.
研究的目的:
- 调查归因于肥胖的内皮变化是否实际上是由OSA引起的.
- 评估OSA对血管炎症,氧化应激和内皮功能的影响.
- 评估持续正气道压力 (CPAP) 治疗对OSA患者内皮功能障碍的影响.
主要方法:
- 71名受试者 (正常体重至肥胖) 接受了多睡眠图.
- 在内皮细胞中量化核因子-kappaB和铁的表达,用于炎症和氧化应激.
- 测量了内皮氧化合成酶 (eNOS),化 eNOS 和臂动脉流介导扩张的内皮功能.
- 在OSA患者接受CPAP治疗4周后评估的变化.
主要成果:
- 与没有OSA的受试者相比,OSA患者表现出较低的eNOS和酸化eNOS表达和受损的流媒体扩张.
- 在OSA患者中,尼铁的表达显著更高.
- 在附着OSA患者中,CPAP疗法改善了流媒体扩张和eNOS表达,同时降低了尼托铁和核因子-kappaB.
结论:
- 未经治疗的OSA是肥胖个体血管内皮功能障碍,炎症和氧化应激的主要驱动因素.
- 与OSA相比,肥胖本身对内皮功能的影响不那么大.
- CPAP疗法有效地逆转与OSA相关的内皮功能障碍和炎症.
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