发作性低氧对非快速动眼睡眠期低碳酸血症性中枢性睡眠呼吸暂停易感性的影响。
Effect of episodic hypoxia on the susceptibility to hypocapnic central apnea during NREM sleep.
机构信息
Medical Service, John D. Dingell Veterans Affairs Medical Center, Detroit, MI 48201, USA.
出版信息
J Appl Physiol (1985). 2010 Feb;108(2):369-77. doi: 10.1152/japplphysiol.00308.2009. Epub 2009 Nov 25.
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 PCO(2) (Pet(CO(2))) demarcating the central apnea. The difference between the AT and baseline Pet(CO(2)) 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(CO(2)) (DeltaV(I)/ DeltaPet(CO(2))) was defined as the hypocapnic ventilatory response. We studied the eupneic Pet(CO(2)), AT Pet(CO(2)), 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 (DeltaV(I)/DeltaSa(O(2))) during the EH trials. V(I) increased from 6.2 +/- 0.4 l/min during the pre-EH control to 7.9 +/- 0.5 l/min during EH and remained elevated at 6.7 +/- 0.4 l/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, DeltaV(I)/DeltaPet(CO(2)) was higher compared with the baseline (3.3 +/- 0.6 vs. 1.8 +/- 0.3 l x min(-1) x mmHg(-1), P < 0.001), indicative of an increased hypocapnic ventilatory response. However, there was no significant change in the hypoxic ventilatory response (DeltaV(I)/DeltaSa(O(2))) 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.
我们假设，发作性低氧（EH）会导致化学感受器特性发生改变，从而可能促进睡眠中人类中枢性呼吸暂停的发生。我们使用经鼻非侵入性正压机械通气，在 11 名健康受试者稳定的非快速动眼睡眠期间，在经历 EH 之前和之后诱发低碳酸性中枢性呼吸暂停，EH 由 15 个 1 分钟的等碳酸缺氧发作组成（平均 O2 饱和度/发作：87.0 +/- 0.5%）。呼吸暂停阈值（AT）定义为绝对测量的呼气末 PCO2（PetCO2），标志着中枢性呼吸暂停。在机械通气开始之前立即测量的 AT 与基线 PetCO2 之间的差异定义为 CO2 储备。PetCO2 变化 1mmHg 时通气量（V I）的变化（DeltaV I/DeltaPetCO2）定义为低碳酸性通气反应。我们研究了 EH 暴露前后的安静 PetCO2、AT PetCO2、CO2 储备和低碳酸性通气反应。我们还测量了低氧性通气反应，定义为动脉血氧饱和度相应变化时通气量的变化（DeltaV I/DeltaSa（O2））在 EH 试验期间。EH 前的基础状态下，V I 从 6.2 +/- 0.4 l/min 增加到 EH 期间的 7.9 +/- 0.5 l/min，并且在 EH 后的恢复期内仍保持在 6.7 +/- 0.4 l/min（P < 0.05），表明存在长期易化。EH 后 AT 不变，但 CO2 储备从 EH 前的-3.1 +/- 0.5mmHg 显著下降至 EH 后的-2.3 +/- 0.4mmHg（P < 0.001）。在 EH 后的恢复期，DeltaV I/DeltaPetCO2 与基线相比升高（3.3 +/- 0.6 对 1.8 +/- 0.3 l x min-1 x mmHg-1，P < 0.001），表明低碳酸性通气反应增加。然而，EH 期间本身的低氧性通气反应（DeltaV I/DeltaSa（O2））没有明显变化。总之，尽管存在通气长期易化，但 EH 后低碳酸性通气反应的增加导致 CO2 储备显著下降。这种形式的呼吸可塑性可能会破坏呼吸稳定性并促进中枢性呼吸暂停。
Zotero 插件