Halker R B, Pierchala L A, Badr M S
Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University, 3 Hudson, Harper University Hospital, 3990 John R, Detroit, MI 48201, USA.
Sleep Breath. 2007 Sep;11(3):165-70. doi: 10.1007/s11325-006-0099-1.
Termination of hypoxia results in a transient ventilatory decline referred to as post-hypoxic ventilatory decline (PHVD). We wished to determine whether PHVD is due to changes in ventilatory motor output or upper airway mechanics. We studied 19 healthy normal subjects (15 men, 4 women) during stable non-REM (NREM) sleep. Subjects were exposed to multiple episodes of brief (3 min) hypoxia that terminated with one breath of 100% FI(O2). Minute ventilation (V (I)), tidal volume (V (T)), timing, and upper airway resistance (R (ua)) were measured during the control, hypoxia, and for the first six breaths immediately after cessation of hypoxia. In addition, we measured diaphragmatic electromyograms (EMGdia) via surface electrodes in four subjects. V (I) and V (T) decreased during the recovery period to a nadir of 81 and 83% of room air control, respectively. However, there was no significant change in respiratory frequency or upper airway resistance during the post-hypoxic recovery period. Decreased V (I) was associated with a comparable decrease in EMGdia. We conclude that: (1) PHVD occurs in normal humans during NREM sleep, (2) there is no evidence of post-hypoxic frequency decline in humans during NREM sleep, and (3) PHVD is centrally mediated and not driven by upper airway mechanics.
缺氧终止会导致一种短暂的通气量下降,称为缺氧后通气量下降(PHVD)。我们希望确定PHVD是由于通气运动输出的变化还是上呼吸道力学的变化所致。我们在稳定的非快速眼动(NREM)睡眠期间研究了19名健康正常受试者(15名男性,4名女性)。受试者经历了多次短暂(3分钟)的缺氧发作,以一次100%氧浓度的呼吸结束。在对照期、缺氧期以及缺氧停止后的前六次呼吸期间,测量了分钟通气量(V̇I)、潮气量(VT)、时间和上呼吸道阻力(Rua)。此外,我们通过表面电极在四名受试者中测量了膈肌肌电图(EMGdia)。在恢复期,V̇I和VT分别降至室内空气对照值的81%和83%的最低点。然而,在缺氧后恢复期,呼吸频率或上呼吸道阻力没有显著变化。V̇I的降低与EMGdia的相应降低相关。我们得出结论:(1)PHVD在正常人类的NREM睡眠期间发生,(2)没有证据表明人类在NREM睡眠期间存在缺氧后频率下降,(3)PHVD是由中枢介导的,而非由上呼吸道力学驱动。