Rist K E, Daubenspeck J A, McGovern J F
Respir Physiol. 1986 Feb;63(2):241-56. doi: 10.1016/0034-5687(86)90117-9.
We observed that ventilation fell and end-tidal CO2 rose in the change from wakefulness to non-REM (NREM) sleep in 4 normal human subjects studied on two nights each. We hypothesized that the observed ventilatory depression was due to effects of sleep both upon the central respiratory neural output and upon the mechanical respiratory pump. Both the central controller response to CO2, as measured by diaphragmatic and intercostal EMG activity, and the ability of the respiratory pump in effecting ventilation in response to diaphragmatic or intercostal activation, as measured by the relationship between the EMG activities and minute ventilation, are reduced in NREM sleep. We describe a general method of apportioning the separate effects of sleep, or other factors, upon the central respiratory controller, the respiratory mechanical pump, and the metabolic rate, in determining the total observed increase in end-tidal CO2.
我们观察了4名正常受试者，每人在两个晚上进行研究，发现在从清醒状态转变为非快速眼动（NREM）睡眠时，通气量下降，呼气末二氧化碳分压上升。我们推测，观察到的通气抑制是由于睡眠对中枢呼吸神经输出和机械呼吸泵均产生了影响。在NREM睡眠中，无论是通过膈肌和肋间肌肌电图活动测量的中枢控制器对二氧化碳的反应，还是通过肌电图活动与分钟通气量之间的关系测量的呼吸泵响应膈肌或肋间肌激活实现通气的能力，均会降低。我们描述了一种通用方法，用于在确定呼气末二氧化碳分压总体观察到的升高时，分摊睡眠或其他因素对中枢呼吸控制器、呼吸机械泵和代谢率的单独影响。
