Effect of episodic hypoxia on the susceptibility to hypocapnic central apnea during NREM sleep
Effect of episodic hypoxia on the susceptibility to hypocapnic central apnea during NREM sleep
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DOI：
10.1152/japplphysiol.00308.2009
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发表时间：
2010-02-01
影响因子：
3.3
通讯作者：
Badr, M. Safwan
中科院分区：
文献类型：
--
作者：
Chowdhuri, Susmita;Shanidze, Irina;Badr, M. Safwan
Chowdhuri S，Shanidze I，Pierchala L，Belen D，Mateika JH，Badr MS.在NREM睡眠期间，发作性缺氧对低碳酸血症中枢性呼吸暂停易感性的影响。J Appl Physiol 108：369-377，2010.首次发表于2009年11月25日; doi：10.1152/japplphysiol.00308.2009。我们假设，发作性缺氧（EH）导致化学反射特性的改变，这可能会促进睡眠中人类中枢性呼吸暂停的发展。我们在11名健康受试者暴露于高血压之前和之后的稳定非快速眼动睡眠中，使用鼻无创正压机械通气诱导低碳酸血症性中枢性呼吸暂停，其中包括15次1分钟的等碳酸血症性缺氧（平均O（2）饱和度/发作：87.0 +/- 0.5%）。呼吸暂停阈值（AT）被定义为绝对测量的呼气末P（CO2）（PET（CO2）），以区分中枢性呼吸暂停。机械通气开始前即刻测量的AT和基线PET（CO2）之间的差异定义为CO（2）储备。每分钟通气量（V（I））随PET（CO2）变化的变化（Δ V（I）/Δ PET（CO2））定义为低碳酸血症缓解反应。观察EH暴露前后正常肺PET（CO2）、AT PET（CO2）、CO（2）储备和低碳酸血症反应。我们还测量了缺氧性呼吸反应，定义为EH试验期间动脉血氧饱和度相应变化的V（I）变化（Δ V（I）/Δ Sao（2））。V（I）从EH前对照的6.2 ± 0.41/min增加到EH期间的7.9 ± 0.51/min，并且在EH后恢复期保持在6.7 ± 0.41/min的升高（P < 0.05），指示长期易化。AT在EH后无变化，但CO（2）储备从EH前的-3.1 ± 0.5mmHg降至EH后的-2.3 ± 0.4mmHg（P < 0.001）。在EH后恢复期，Delta V（I）/Delta PET（CO2）高于基线值（3.3 +/- 0.6 vs. 1.8 +/- 0.3 1.min（1）.mmHg（1），P < 0.001），表明低碳酸血症缓解反应增加。然而，在EH期间本身，低氧缓解反应（Δ V（I）/Δ Sa（O2））没有显著变化。总之，尽管存在代偿性长时程易化，但暴露于高血压后低碳酸血症代偿性反应的增加引起CO（2）储备的显著降低。这种形式的呼吸可塑性可能会使呼吸不稳定，并促进中枢性呼吸暂停。
Chowdhuri S, Shanidze I, Pierchala L, Belen D, Mateika JH, Badr MS. Effect of episodic hypoxia on the susceptibility to hypocapnic central apnea during NREM sleep. J Appl Physiol 108: 369-377, 2010. First published November 25, 2009; doi:10.1152/japplphysiol.00308.2009.-We hypothesized that episodic hypoxia (EH) leads to alterations in chemoreflex characteristics that might promote the development of central apnea in sleeping humans. We used nasal noninvasive positive pressure mechanical ventilation to induce hypocapnic central apnea in 11 healthy participants during stable nonrapid eye movement sleep before and after an exposure to EH, which consisted of fifteen 1-min episodes of isocapnic hypoxia (mean O(2) saturation/episode: 87.0 +/- 0.5%). The apneic threshold (AT) was defined as the absolute measured end-tidal P(CO2) (PET(CO2)) demarcating the central apnea. The difference between the AT and baseline PET(CO2) measured immediately before the onset of mechanical ventilation was defined as the CO(2) reserve. The change in minute ventilation (V(I)) for a change in PET(CO2) (Delta V(I)/Delta PET(CO2)) was defined as the hypocapnic ventilatory response. We studied the eupneic PET(CO2), AT PET(CO2), CO(2) reserve, and hypocapnic ventilatory response before and after the exposure to EH. We also measured the hypoxic ventilatory response, defined as the change in V(I) for a corresponding change in arterial O(2) saturation (Delta V(I)/Delta Sao(2)) during the EH trials. V(I) increased from 6.2 +/- 0.41/min during the pre-EH control to 7.9 +/- 0.51/min during EH and remained elevated at 6.7 +/- 0.41/min the during post-EH recovery period (P < 0.05), indicative of long-term facilitation. The AT was unchanged after EH, but the CO(2) reserve declined significantly from -3.1 +/- 0.5 mmHg pre-EH to -2.3 +/- 0.4 mmHg post-EH (P < 0.001). In the post-EH recovery period, Delta V(I)/Delta PET(CO2) was higher compared with the baseline (3.3 +/- 0.6 vs. 1.8 +/- 0.3 1.min (1).mmHg (1), P < 0.001), indicative of an increased hypocapnic ventilatory response. However, there was no significant change in the hypoxic ventilatory response (Delta V(I)/Delta Sa(O2)) during the EH period itself. In conclusion, despite the presence of ventilatory long-term facilitation, the increase in the hypocapnic ventilatory response after the exposure to EH induced a significant decrease in the CO(2) reserve. This form of respiratory plasticity may destabilize breathing and promote central apneas.