阻塞性睡眠呼吸暂停与呼吸调节功能异常

阻塞性睡眠呼吸暂停(OSA)的发病机制尚不明确,可能与呼吸中枢控制功能异常有关。除少数白天并发肺泡通气不足者外,大部分OSA患者在清醒时的呼吸中枢低氧及高CO_2反应性与正常人无差异。进入睡眠状态后,OSA患者呼吸中枢的敏感性在各睡眠时相均降低,其中枢呼吸驱动在NREM Ⅰ期、Ⅱ期及REM睡眠期减弱,特别是伴白天CO_2潴留者呼吸中枢的反应性几乎消失,经夜间持续气道正压通气(CPAP)治疗后,部分患者的中枢反应性可逐渐升高,提示这种改变可能继发于长期睡眠呼吸暂停引起的低氧、高CO_2及睡眠紊乱。动物实验还发现,呼吸中枢的化学反应性与遗传有关,基因缺陷可以引起小鼠的呼吸暂停,说明OSA患者中枢反应性低下也受遗传因素的影响。明确呼吸调节功能异常在OSA发生中的重要作用对选择内科治疗方案,特别是无创性机械通气治疗有指导意义。

Obstructive sleep apnea and the breathing control dysfunction

Impairment of respiration regulation may play an important role in the development of obstrucitve sleep apnea (OSA) .Most of the patients with OSA have normal responses to hypoxia and hypercapnia during wakefulness, but have depressed chemoresponsiveness in both nan - rapid eye movement and rapid eye movement sleep.Treatment with CPAP can improve the waketime alveolar ventilation as well as the chemo -responsiveness in hypercapnic OSA patients.This indicates the depressed chemoresponsiveness may be a response to sleep disordered breathing. We also showed a strain - related occurrence of apnea in inbred C57BL/6J and A/J mice, which have different chemoresponsiveness , indicating a genetic influence on OSA. These studies support the rationale of treating OSA with non - invasive ventilation.