在阻塞性睡眠呼吸暂停中,上呼吸道微循环的重塑不是由内皮细胞激活驱动的
Kristine Fahl1, Thais Mauad2, Jôse M de Brito2
1Department of Otolaryngology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Avenida Dr. Eneas de Carvalho Aguiar 255, 6° Andar, Sala 6167, Sao Paulo, SP, CEP 05403-000, Brazil.
年轻成年人的阻塞性睡眠呼吸暂停 (OSA) 可能导致喉中的微血管向外加厚,而不是增加炎症. 这表明机械变化,而不是内皮激活,在OSA中驱动微循环重塑.
科学领域:
- 心血管生理学心血管生理学
- 睡眠医学 睡眠医学
- 血管生物学 血管生物学
背景情况:
- 微循环对于调节血流阻力至关重要.
- 阻塞性睡眠呼吸暂停 (OSA) 涉及上呼吸道问题,通过内皮激活,剪切应力和振动影响微循环.
- 这些因素对OSA微循环反应和重塑的影响尚不清楚.
研究的目的:
- 为了研究患有OSA的年轻,非肥胖成年人的喉肌肉中的微循环变化.
- 评估与OSA严重程度相关的动脉小胞形态测量和内皮激活标志物.
主要方法:
- 分析了来自非肥胖,年轻成人OSA患者的喉肌肉组织.
- 评估了动脉形态测量,并量化了内皮激活标记物 (8-异素,VCAM-1,E-选择素,VEGF,内皮素-1,ESM-1).
- 检查了呼吸暂停-呼吸暂停指数和动脉壁厚度之间的相关性.
主要成果:
- 与轻度OSA患者相比,严重OSA患者的动脉壁比轻度OSA患者更厚,表明没有光线减少的外向增大.
- 在呼吸暂停-呼吸暂停指数和动脉壁厚度之间发现了正相关性.
- 没有观察到内皮激活标志物的显着增加,在动脉壁或肌肉组织中增加OSA严重程度.
结论:
- 在年轻的,非肥胖的成年人中,严重的OSA似乎会诱导适应性,向外的微循环缩,可能是由改变的剪切应力等机械因素驱动的.
- 在这个人群中,内皮激活标志物不会随着OSA的严重程度而增加.
- 这些发现表明,机械驱动的重塑,而不是炎症,可能是年轻OSA患者微循环变化的特征,这对OSA管理有影响.
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