Sivam Sheila, Witting Paul K, Hoyos Camilla M, Maw Aung M, Yee Brendon J, Grunstein Ronald R, Phillips Craig L
Sleep & Circadian Research Group, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW, Australia.
Discipline of Sleep Medicine, Sydney Medical School, The University of Sydney, NSW, Australia.
J Sleep Res. 2015 Jun;24(3):339-45. doi: 10.1111/jsr.12271. Epub 2014 Dec 22.
Dyslipidaemia and increased oxidative stress have been reported in severe obstructive sleep apnea, and both may be related to the development of cardiovascular disease. We have previously shown in a randomized crossover study in patients with moderate to severe obstructive sleep apnea that therapeutic continuous positive airway pressure treatment for 8 weeks improved postprandial triglycerides and total cholesterol when compared with sham continuous positive airway pressure. From this study we have now compared the effect of 8 weeks of therapeutic continuous positive airway pressure and sham continuous positive airway pressure on oxidative lipid damage and plasma lipophilic antioxidant levels. Unesterified cholesterol, esterified unsaturated fatty acids (cholesteryl linoleate: C18:2; and cholesteryl arachidonate: C20:4; the major unsaturated and oxidizable lipids in low-density lipoproteins), their corresponding oxidized products [cholesteryl ester-derived lipid hydroperoxides and hydroxides (CE-O(O)H)] and antioxidant vitamin E were assessed at 20:30 hours before sleep, and at 06:00 and 08:30 hours after sleep. Amongst the 29 patients completing the study, three had incomplete or missing [CE-O(O)H] data. The mean apnea -hypopnoea index, age and body mass index were 38 per hour, 49 years and 32 kg m(-2) , respectively. No differences in lipid-based oxidative markers or lipophilic antioxidant levels were observed between the continuous positive airway pressure and sham continuous positive airway pressure arms at any of the three time-points [unesterified cholesterol 0.01 mm, P > 0.05; cholesteryl linoleate: C18:2 0.05 mm, P > 0.05; cholesteryl arachidonate: C20:4 0.02 mm, P = 0.05; CE-O(O)H 2.5 nm, P > 0.05; and lipid-soluble antioxidant vitamin E 0.03 μm, P > 0.05]. In this study, accumulating CE-O(O)H, a marker of lipid oxidation, does not appear to play a role in oxidative stress in obstructive sleep apnea.
严重阻塞性睡眠呼吸暂停患者中已报告存在血脂异常和氧化应激增加，两者都可能与心血管疾病的发生有关。我们之前在一项针对中重度阻塞性睡眠呼吸暂停患者的随机交叉研究中表明，与假持续气道正压通气相比，治疗性持续气道正压通气治疗8周可改善餐后甘油三酯和总胆固醇水平。在这项研究中，我们现在比较了8周的治疗性持续气道正压通气和假持续气道正压通气对氧化脂质损伤和血浆亲脂性抗氧化剂水平的影响。在睡前20:30以及睡眠后06:00和08:30评估未酯化胆固醇、酯化不饱和脂肪酸（胆固醇亚油酸酯：C18:2；以及胆固醇花生四烯酸酯：C20:4；低密度脂蛋白中的主要不饱和且可氧化脂质）、它们相应的氧化产物[胆固醇酯衍生的脂质氢过氧化物和氢氧化物（CE-O(O)H）]以及抗氧化维生素E。在完成研究的29名患者中，有3名患者的[CE-O(O)H]数据不完整或缺失。平均呼吸暂停低通气指数、年龄和体重指数分别为每小时38次、49岁和32 kg m(-2)。在三个时间点的任何一个时间点，持续气道正压通气组和假持续气道正压通气组之间在基于脂质的氧化标志物或亲脂性抗氧化剂水平方面均未观察到差异[未酯化胆固醇0.01 mmol/L，P>0.05；胆固醇亚油酸酯：C18:2 0.05 mmol/L，P>0.05；胆固醇花生四烯酸酯：C20:4 0.02 mmol/L，P = 0.05；CE-O(O)H 2.5 nmol/L，P>0.05；以及脂溶性抗氧化维生素E 0.03 μmol/L，P>0.05]。在这项研究中，作为脂质氧化标志物的累积CE-O(O)H似乎在阻塞性睡眠呼吸暂停的氧化应激中不起作用。
