Worsening of central sleep apnea at high altitude-a role for cerebrovascular function

Worsening of central sleep apnea at high altitude-a role for cerebrovascular function
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DOI:
10.1152/japplphysiol.01462.2012
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发表时间:
2013-04-01
影响因子:
3.3
通讯作者:
Ainslie, Philip N.
Ainslie, Philip N.
中科院分区:
医学2区
文献类型:
--
作者:
Burgess, Keith R.;Lucas, Samuel J. E.;Ainslie, Philip N.

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Burgess KR, Lucas SJ, Shepherd K, Dawson A, Swart M, Thomas KN, Lucas RA, Donnelly J, Peebles KC, Basnyat R, Ainslie PN。中枢性睡眠呼吸暂停在高海拔地区的恶化-脑血管功能的作用。中国生物医学工程学报,2014,31(2):444 - 444。首次发表于2012年2月21日;doi: 10.1152 / japplphysiol.01462.2012。-尽管在高海拔地区睡眠时周期性呼吸几乎普遍存在,但海拔和环境适应的可能机制和独立影响尚未明确报道。2005年的数据表明,睡眠开始时脑血流量(CBF)的下降与当晚中枢性睡眠呼吸暂停的严重程度之间存在显著关系。我们怀疑CBF在部分驯化过程中会下降。因此,我们假设CBF及其反应性的减少会使部分适应环境后睡眠期间的周期性呼吸恶化。反复测量清醒时呼吸和脑血流反应性,清醒时动脉血气。在到达海拔5050米时(第2-4天)和部分适应后(第12-15天),对12名受试者进行夜间多导睡眠仪检查。呼吸暂停低通气指数(AHI)由第2 ~ 4天的77 +/- 49上升至第12 ~ 15天的116 +/- 21 (P = 0.01)。初次到达时的AHI与CBF的显著升高(+28%,68 +/- 11至87 +/- 17 cm/s; P < 0.05)及其对Pa-CO2变化的反应性(90%,2.0 +/- 0.6至3.8 +/- 1.5 cm)相关。(1)。mmHg(-1)高碳酸血症,1.9 +/- 0.4 ~ 4.1 +/- 0.9 cm。(1)。低碳酸血症mmHg(-1) [P < 0.05]。10天后,升高消退,AHI恶化。在高海拔睡眠期间,平均脑血流速度(CBFv)出现了较大的振荡,与第12-15天相比,CBFv初始值(峰值为96 cm/s vs峰值为71 cm/s)提高了35%。我们的新发现表明,在最初上升到高海拔时,CBF的升高及其对二氧化碳的反应性可能对睡眠期间周期性呼吸的发展提供了保护作用(可能通过调节中枢P-CO2的变化)。
Burgess KR, Lucas SJ, Shepherd K, Dawson A, Swart M, Thomas KN, Lucas RA, Donnelly J, Peebles KC, Basnyat R, Ainslie PN. Worsening of central sleep apnea at high altitude-a role for cerebrovascular function. J Appl Physiol 114: 1021-1028, 2013. First published February 21, 2012; doi:10.1152/japplphysiol.01462.2012.-Although periodic breathing during sleep at high altitude occurs almost universally, the likely mechanisms and independent effects of altitude and acclimatization have not been clearly reported. Data from 2005 demonstrated a significant relationship between decline in cerebral blood flow (CBF) at sleep onset and subsequent severity of central sleep apnea that night. We suspected that CBF would decline during partial acclimatization. We hypothesized therefore that reductions in CBF and its reactivity would worsen periodic breathing during sleep following partial acclimatization. Repeated measures of awake ventilatory and CBF responsiveness, arterial blood gases during wakefulness. and overnight polysomnography at sea level, upon arrival (days 2-4), and following partial acclimatization (days 12-15) to 5,050 m were made on 12 subjects. The apnea-hypopnea index (AHI) increased from to 77 +/- 49 on days 2-4 to 116 +/- 21 on days 12-15 (P = 0.01). The AHI upon initial arrival was associated with marked elevations in CBF (+28%, 68 +/- 11 to 87 +/- 17 cm/s; P < 0.05) and its reactivity to changes in Pa-CO2 [>90%, 2.0 +/- 0.6 to 3.8 +/- 1.5 cm . s(-1) . mmHg(-1) hypercapnia and 1.9 +/- 0.4 to 4.1 +/- 0.9 cm . s(-1) . mmHg(-1) for hypocapnia (P < 0.05)]. Over 10 days, the increases resolved and AHI worsened. During sleep at high altitude large oscillations in mean CBF velocity (CBFv) occurred, which were 35% higher initially (peak CBFv = 96 cm/s vs. peak CBFv = 71 cm/s) than at days 12-15. Our novel findings suggest that elevations in CBF and its reactivity to CO2 upon initial ascent to high altitude may provide a protective effect on the development of periodic breathing during sleep (likely via moderating changes in central P-CO2).