Xie A, Rankin F, Rutherford R, Bradley T D
Sleep Research Laboratory, Queen Elizabeth Hospital, Toronto, Ontario, Canada.
J Appl Physiol (1985). 1997 Mar;82(3):918-26. doi: 10.1152/jappl.1997.82.3.918.
We hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.
我们推测，动脉血二氧化碳分压（PaCO₂）降至呼吸暂停阈值以下在特发性中枢性睡眠呼吸暂停综合征（ICSAS）的发病机制中起关键作用。如果是这样，我们推断提高PaCO₂将消除这些患者的呼吸暂停。因此，对ICSAS患者进行了四次夜间研究，期间测量了呼气末二氧化碳分数和经皮二氧化碳分压：在室内空气呼吸期间（N1）、交替进行室内空气和二氧化碳呼吸期间（N2）、整夜进行二氧化碳呼吸期间（N3）以及通过面罩整夜增加死腔期间（N4）。中枢性呼吸暂停总是先于呼气末二氧化碳分数降低。给予富含二氧化碳的气体混合物和增加死腔均导致经皮二氧化碳分压升高1至3托，这几乎消除了呼吸暂停和呼吸浅慢；它们从N1时的43.7±7.3次呼吸暂停和呼吸浅慢/小时降至N3时的5.8±0.9次呼吸暂停和呼吸浅慢/小时（P<0.005），从室内空气呼吸时的43.8±6.9次呼吸暂停和呼吸浅慢/小时降至N2时吸入二氧化碳期间睡眠时的5.9±2.5次呼吸暂停和呼吸浅慢/小时（P<0.01），在N4期间患者通过增加的死腔呼吸时降至室内空气水平的11.6%（P<0.005）。由于通过两种不同方法提高PaCO₂几乎消除了中枢性睡眠呼吸暂停，我们得出结论，ICSA睡眠期间的中枢性呼吸暂停是由于PaCO₂降至呼吸暂停阈值以下所致。
