Tokunou Tomotake, Yoshikawa Tomoko, Yoshioka Yasuko, Ando Shin-Ichi
Division of Basic Medical Science and Fundamental Nursing, Department of Nursing, Fukuoka Nursing College, 2-15-1, Tamura, Sawara-ku, Fukuoka, 814-0193 Japan.
Division of Cardiology, Department of Medicine, Fukuoka Dental College Hospital, Fukuoka, Japan.
Sleep Biol Rhythms. 2024 Jun 15;22(4):499-504. doi: 10.1007/s41105-024-00537-w. eCollection 2024 Oct.
Intermittent hypoxia in sleep apnea syndrome (SAS) patients increases the oxidative stress and can cause serious cardiovascular diseases such as hypertension or atherosclerotic diseases through endothelial dysfunction. The evaluation of risk caused by oxidative stress, however, is not easy in a clinical setting. Thus, we intended to evaluate the changes in oxidative stress by SAS treatment using a simple method that can be easily used in the clinical testing. We enrolled 42 consecutive newly diagnosed severe SAS patients (30 men). Reactive oxygen species metabolites (d-ROMs) for oxidative stress and biological antioxidant (BAP) in blood samples were estimated using FREE Carrio Duo before and 3 months after continuous positive airway pressure (CPAP) treatment. SAS parameters were obtained by polysomnography before CPAP and endothelial function was measured twice as well. The body mass index and apnea hypopnea index (AHI) were 29.1 ± 5.3 and 57.9 ± 19.7/h. The d-ROMs and BAP were 317.4 ± 71.8 CARR U and 2121.2 ± 299.6 μmol/L. Although no significant correlation was found between hypoxia parameters and d-ROMs or BAP before CPAP treatment, we found a significant negative correlation between basal AHI or basal oxygen desaturation index representing intermittent hypoxia and the change in d-ROMs ( = - 0.31, = 0.046/ = - 0.33, = 0.03) and between the change in SpO < 90% duration (min) representing continuous hypoxia and the change in BAP ( = - 0.35, = 0.03) after CPAP treatment. The changes in d-ROM and BAP might reflect the different kind of reduction of oxidative stress by CPAP treatment and, thus, can be used as handy indicators of the treatment effect.
睡眠呼吸暂停综合征（SAS）患者的间歇性缺氧会增加氧化应激，并可通过内皮功能障碍导致严重的心血管疾病，如高血压或动脉粥样硬化疾病。然而，在临床环境中评估氧化应激所造成的风险并不容易。因此，我们打算使用一种可在临床检测中轻松应用的简单方法，来评估SAS治疗引起的氧化应激变化。我们连续招募了42例新诊断的重度SAS患者（30名男性）。在持续气道正压通气（CPAP）治疗前和治疗3个月后，使用FREE Carrio Duo检测血液样本中氧化应激的活性氧代谢产物（d-ROMs）和生物抗氧化剂（BAP）。通过多导睡眠图在CPAP治疗前获取SAS参数，并且也对内皮功能进行了两次测量。体重指数和呼吸暂停低通气指数（AHI）分别为29.1±5.3和57.9±19.7次/小时。d-ROMs和BAP分别为317.4±71.8 CARR U和2121.2±299.6μmol/L。虽然在CPAP治疗前未发现缺氧参数与d-ROMs或BAP之间存在显著相关性，但我们发现代表间歇性缺氧的基础AHI或基础氧去饱和指数与d-ROMs的变化之间存在显著负相关（r = - 0.31，P = 0.046/r = - 0.33，P = 0.03），并且在CPAP治疗后，代表持续性缺氧的SpO₂<90%持续时间（分钟）的变化与BAP的变化之间存在显著负相关（r = - 0.35，P = 0.03）。d-ROM和BAP的变化可能反映了CPAP治疗对氧化应激不同程度的减轻作用，因此可作为治疗效果的便捷指标。
