Long-term facilitation of ventilation following acute continuous hypoxia in awake humans during sustained hypercapnia
Long-term facilitation of ventilation following acute continuous hypoxia in awake humans during sustained hypercapnia
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DOI：
10.1113/jphysiol.2012.236109
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发表时间：
2012-10-01
影响因子：
5.5
通讯作者：
Balanos, George M.
中科院分区：
文献类型：
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作者：
Griffin, Harry S.;Pugh, Keith;Balanos, George M.
在清醒的人类中，当二氧化碳维持在正常水平以上时，暴露于急性间歇性缺氧会导致通气持续升高，当恢复正常呼吸时，通气持续升高。在这项研究中，我们已经证明，当二氧化碳维持在正常水平以上时，暴露于急性持续缺氧也会导致恢复正常呼吸时通气的持续升高。急性间歇缺氧和急性持续缺氧后通气的持续升高是由颈动脉体活动增加以外的机制维持的。这些结果有助于加深我们对人类呼吸控制的理解，并可能有助于未来开发呼吸控制疾病的治疗方法，如阻塞性睡眠呼吸暂停。在清醒的人类中，急性间歇性缺氧（AIH）后的长期通气促进（vLTF）仅在CO2维持在正能量水平以上时表达。急性持续缺氧（ACH）后未见vLTF的报道，也不知道这是否可能被升高的CO2所掩盖。12名健康的参与者完成了三项试验。在所有试验中，CO2的潮汐末压比正常水平升高了45毫米汞柱。在试验1 （AIH）中，参与者暴露于8次4分钟的缺氧发作。在试验2 （ACH）中，参与者暴露于持续缺氧32分钟。在试验3（对照）中，参与者始终暴露于氧气中。为了评估颈动脉体（CB）在观察到的通气反应中的作用，每次试验前后的颈动脉体传入放电都被高氧暂时抑制。每分钟通气量（）在所有试验中均有所增加，但试验1和试验2与试验3相比显著增加（试验1:4.96 +/- 0.87，试验2:5.07 +/- 0.7，试验3:2.55 +/- 0.98 l min-1, P < 0.05）。在所有试验中，高氧在基线和恢复时的减弱程度相似（试验1:3.0 +/- 0.57 vs. 3.27 +/- 0.68，试验2:1.97 +/- 0.62 vs. 2.56 +/- 0.62，试验3:2.23 +/- 0.49 vs. 2.15 +/- 0.55 l min-1, P < 0.05）。数据为平均值+/- SEM。在二氧化碳浓度升高的清醒人群中，乙酰胆碱引起的通气持续增加与AIH引起的通气增加相当。然而，随着二氧化碳浓度的升高，通风中的逐渐正漂移约占这一明显vLTF的一半。此外，我们的数据支持CB不直接参与维护vLTF的观点。
Key points In awake humans, when CO2 is maintained above normal levels, exposure to acute intermittent hypoxia causes a sustained elevation in ventilation that persists when normoxic breathing is resumed. In this study we have demonstrated that when CO2 is maintained above normal levels, exposure to acute continuous hypoxia also causes a sustained elevation in ventilation when normoxic breathing is resumed. This sustained elevation in ventilation following both acute intermittent hypoxia and acute continuous hypoxia is maintained by mechanisms other than increased activity of the carotid body. These results help develop our understanding of respiratory control in humans and may aid future development of treatments for respiratory control disorders, such as obstructive sleep apnoea. Abstract In awake humans, long-term facilitation of ventilation (vLTF) following acute intermittent hypoxia (AIH) is only expressed if CO2 is maintained above normocapnic levels. vLTF has not been reported following acute continuous hypoxia (ACH) and it is not known whether this might be unmasked by elevated CO2. Twelve healthy participants completed three trials. In all trials end-tidal pressure of CO2 was elevated 45 mmHg above normocapnic levels. During Trial 1 (AIH) participants were exposed to eight 4 min episodes of hypoxia. During Trial 2 (ACH) participants were exposed to continuous hypoxia for 32 min. In Trial 3 (Control) participants were exposed to euoxia throughout. To assess the contribution of the carotid body (CB) in observed ventilatory responses, CB afferent discharge before and after each trial was transiently inhibited with hyperoxia. Minute ventilation () increased following all trials, but was significantly greater in Trials 1 and 2 when compared with Trial 3 (Trial 1: 4.96 +/- 0.87, Trial 2: 5.07 +/- 0.7, Trial 3: 2.55 +/- 0.98 l min-1, P < 0.05). Hyperoxia attenuated to a similar extent in baseline and recovery in all trials (Trial 1: 3.0 +/- 0.57 vs. 3.27 +/- 0.68, Trial 2: 1.97 +/- 0.62 vs. 2.56 +/- 0.62, Trial 3: 2.23 +/- 0.49 vs. 2.15 +/- 0.55 l min-1, P > 0.05). Data are means +/- SEM. In awake humans with elevated CO2, ACH evokes a sustained increase in ventilation that is comparable to that evoked by AIH. However, a gradual positive drift in ventilation in response to elevated CO2 accounts for approximately half of this apparent vLTF. Additionally, our data support the view that the CB is not directly involved in maintaining vLTF.