Abstract：
Obstructive sleep apnea (OSA) is a prevalent sleep disorder that is associated with increased incidence of chronic musculoskeletal pain. We investigated the mechanism of this association in a mouse model of chronic intermittent hypoxia (CIH) that mimics the repetitive hypoxemias of OSA. After 14 days of CIH, both male and female mice exhibited behaviors indicative of persistent pain, with biochemical markers in the spinal cord dorsal horn and sensory neurons of the dorsal root ganglia consistent with hyperalgesic priming. CIH, but not sleep fragmentation alone, induced an increase in macrophage recruitment to peripheral sensory tissues (sciatic nerve and dorsal root ganglia), an increase in inflammatory cytokines in the circulation, and nociceptor sensitization. Peripheral macrophage ablation blocked CIH-induced hyperalgesic priming. The findings suggest that correcting the hypoxia or targeting macrophage signaling might suppress persistent pain in patients with OSA.
摘要：
阻塞性睡眠呼吸暂停（OSA）是一种常见的睡眠障碍，与慢性肌肉骨骼疼痛的发生率增加有关。我们在模拟OSA重复性低氧血症的慢性间歇性低氧（CIH）小鼠模型中研究了这种关联的机制。CIH14天后，雄性和雌性小鼠都表现出持续性疼痛的行为，脊髓背角和背根神经节的感觉神经元中的生化标记与痛觉过敏引发一致。CIH,但不仅仅是睡眠碎片，诱导巨噬细胞募集到周围感觉组织（坐骨神经和背根神经节）的增加，循环中炎症细胞因子的增加，和伤害性感受器致敏。外周巨噬细胞消融阻断CIH诱导的痛觉过敏引发。研究结果表明，纠正缺氧或靶向巨噬细胞信号可能会抑制OSA患者的持续性疼痛。
