A novel strategy using radical scavengers against intermittent hypoxia-induced oxidative stress in heart, kidney, and brain

与睡眠呼吸暂停相关的间歇性缺氧（IH）会增加心血管疾病发病率和死亡率的风险。本研究表明，IH增加了心脏和肾脏的超氧化物生成、氧化应激和炎症细胞因子的表达，加速了缺氧应激引起的组织变性。吸入氢气（H2）气体可改善脂质代谢，减少氧化应激。此外，氢气可以改善暴露于IH的Bio14.6型心肌病仓鼠恶化的收缩功能。另一方面，使用β 1选择性肾上腺素受体阻滞剂塞利洛尔治疗可抑制IH期间的血压波动，恢复eNOS表达，并减轻IH引起的心脏重构。有趣的是，暴露于IH的肥胖糖尿病小鼠的边缘Fos表达被显著抑制，与镇静和/或抑郁行为体征相关，这可能与糖尿病睡眠呼吸暂停患者的神经心理障碍有关。

Intermittent hypoxia (IH) relevant to sleep apnea is known to increase the risk of cardiovascular morbidity and mortality. This study showed that IH increased superoxide production, oxidative stress, and inflammatory cytokine expression in heart and kidney, accelerating histological degeneration due to hypoxic stress. Inhalation of hydrogen (H2) gas improved lipid metabolism and reduced oxidative stress. Furthermore, H2 gas improved the deteriorated systolic function in Bio14.6 cardiomyopathic hamster exposed to IH. On the other hand, treatment with celiprolol, a beta 1-selective adrenoreceptor blocker, suppressed blood pressure fluctuation during IH, restored eNOS expression, and attenuated cardiac remodeling caused by IH. Intriguingly, limbic Fos expression was significantly suppressed in obese diabetic mice exposed to IH, associated with sedative and/or depressive behavioral signs, which may related to the neuropsychological disturbances in diabetic patients with sleep apnea.