Hypoxic stress and atherosclerosis in patients with sleep apnea-hypopnea syndrome

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）的特征是睡眠期间反复发作的氧饱和度下降。本研究的目的是（1）探讨低氧应激对OSAHS患者外周血单核细胞产生TNF-α和MCP-1的影响，（2）探讨低氧应激对OSAHS患者血浆脂联素（ADPN）的影响。结果：（1）单核细胞分泌TNF-α和MCP-1的增加与OSAHS诱导的低氧应激有关。这种现象可能有助于OSAHS患者动脉粥样硬化的发展。nCPAP治疗3个月可能有助于预防OSAHS患者动脉粥样硬化的发生。（2）血浆中ADPN降低和TNF-α升高与OSAS-OSAS引起的低氧应激有关。短期nCPAP治疗1 d后，OSAHS患者血浆ADPN水平未完全恢复。

Obstructive sleep apnea-hypopnea syndrome(OSAHS) is characterized by recurrent episodes of oxygen desaturation during sleep. In addition, recent studies have shown that OSAHS may be one of the important independent risk factors of cardiovascular diseases.The aim of the present study was (1)to clarify the effect of hypoxic stress on the production of TNF-α and MCP-1 by peripheral blood monocytes, and (2)to investigate the impact of hypoxic stress on plasma adiponectin(ADPN) in patients with OSAHS. We also examined the long-term or the short-term effects of nasal continuous positive airway pressure(nCPAP) on the production of TNF-α and MCP-1, and ADPN.Summary of results ; (1)The elevated production of TNF-α and MCP-1 by monocytes was associated with OSAHS-induced hypoxic stress. This phenomenon may contribute to the development of atherosclerosis in OSAHS. Furthermore, it was suggested that nCPAP therapy for 3 months may be beneficial to the prevention of atherosclerosis in OSAHS. (2)Both reduced ADPN and elevated TNF-α in plasma are associated with OSAS-induced hypoxic stress. The suppressed level of plasma ADPN in OSAHS was not fully recovered by the short-term nCPAP therapy for 1 day.