Impact of repeated daily exposure to intermittent hypoxia and mild sustained hypercapnia on apnea severity.
Impact of repeated daily exposure to intermittent hypoxia and mild sustained hypercapnia on apnea severity.
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DOI：
10.1152/japplphysiol.00702.2011
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发表时间：
2012-02
影响因子：
3.3
通讯作者：
S. Yokhana;D. G. Gerst;Dorothy S. Lee;M. S. Badr;T. Qureshi;J. Mateika
中科院分区：
文献类型：
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作者：
S. Yokhana;D. G. Gerst;Dorothy S. Lee;M. S. Badr;T. Qureshi;J. Mateika
我们研究了睡眠呼吸暂停患者在清醒时暴露于间歇性低氧(IH)是否对睡眠中的呼吸暂停/低通气指数(AHI)产生影响。受试者在持续轻度高碳酸血症的情况下，每天暴露在12次4分钟的低氧中，持续10天。对照组暴露在持续轻度高碳酸血症中，持续时间相似。间歇性低氧方案在第1天和第10天的晚上完成，随后进行睡眠研究。在所有睡眠研究中，使用从呼吸暂停开始到结束的食道压力变化(ΔPes)和呼吸暂停事件后立即的潮气量来测量呼吸动力。在暴露于IH的第1天和第10天，AHI高于基线测量(第1天：基线的1.95±0.42分，P≤0.01，而第10天：1.53±0.24分基线，P<；0.06)。这些指标与IH方案中测量的缺氧性呼吸反应(HVR)相关，但与呼吸机长期促进(VLTF)的大小无关。同样，第1天和第10天的ΔPES和潮气量测量均大于基线(ΔPES：-8.37±0.84vs.-5.90±1.30cmH(2)0，P≤0.04；潮气量：1193.36±101.85 vs.1015.14±119.83 ml，P≤0.01)。但对照组的情况并非如此。有趣的是，轻度高碳酸血症对照组第10天的呼吸暂停指数(0.78±0.13)显著低于基线和第1天(P≤0.0 1)。我们的结论是，暴露于IH引起的HVR增强可能导致睡眠中AHI的增加，而vLTF的启动似乎不会影响呼吸稳定性。最后，我们的结果表明，每天反复暴露于轻度持续性高碳酸血症可能会导致呼吸事件的减少。
We examined whether exposure to intermittent hypoxia (IH) during wakefulness impacted on the apnea/hypopnea index (AHI) during sleep in individuals with sleep apnea. Participants were exposed to twelve 4-min episodes of hypoxia in the presence of sustained mild hypercapnia each day for 10 days. A control group was exposed to sustained mild hypercapnia for a similar duration. The intermittent hypoxia protocol was completed in the evening on day 1 and 10 and was followed by a sleep study. During all sleep studies, the change in esophageal pressure (ΔPes) from the beginning to the end of an apnea and the tidal volume immediately following apneic events were used to measure respiratory drive. Following exposure to IH on day 1 and 10, the AHI increased above baseline measures (day 1: 1.95 ± 0.42 fraction of baseline, P ≤ 0.01, vs. day 10: 1.53 ± 0.24 fraction of baseline, P < 0.06). The indexes were correlated to the hypoxic ventilatory response (HVR) measured during the IH protocol but were not correlated to the magnitude of ventilatory long-term facilitation (vLTF). Likewise, ΔPes and tidal volume measures were greater on day 1 and 10 compared with baseline (ΔPes: -8.37 ± 0.84 vs. -5.90 ± 1.30 cmH(2)0, P ≤ 0.04; tidal volume: 1,193.36 ± 101.85 vs. 1,015.14 ± 119.83 ml, P ≤ 0.01). This was not the case in the control group. Interestingly, the AHI on day 10 (0.78 ± 0.13 fraction of baseline, P ≤ 0.01) was significantly less than measures obtained during baseline and day 1 in the mild hypercapnia control group. We conclude that enhancement of the HVR initiated by exposure to IH may lead to increases in the AHI during sleep and that initiation of vLTF did not appear to impact on breathing stability. Lastly, our results suggest that repeated daily exposure to mild sustained hypercapnia may lead to a decrease in breathing events.