Progressive augmentation and ventilatory long-term facilitation are enhanced in sleep apnoea patients and are mitigated by antioxidant administration
Progressive augmentation and ventilatory long-term facilitation are enhanced in sleep apnoea patients and are mitigated by antioxidant administration
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DOI：
10.1113/jphysiol.2009.178053
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发表时间：
2009-11-15
影响因子：
5.5
通讯作者：
Mateika, Jason H.
中科院分区：
文献类型：
--
作者：
Lee, Dorothy S.;Badr, M. Safwan;Mateika, Jason H.
呼吸运动输出的渐进性增强(PA)和呼吸性长期促进(VLTF)是呼吸可塑性的一种形式，在间歇性低氧中启动。本研究旨在确定与匹配的健康对照组相比，阻塞性睡眠呼吸暂停(OSA)患者的PA和vLTF是否增强。这项研究还旨在确定服用抗氧化剂鸡尾酒是否可以缓解PA和vLTF。13名患有睡眠呼吸暂停的参与者和13名对照组完成了两项试验。在两个试验中，参与者暴露在间歇性低氧中，其中包括12次4分钟的低氧(P-ETO2，50 mm Hg；P-ETCO2，高于基线4 mm Hg)，然后恢复30分钟。在暴露于间歇性低氧之前，参与者以随机方式接受抗氧化剂或安慰剂鸡尾酒。在安慰剂和抗氧化剂试验期间，每分钟通气量的基线测量在组内或组内没有差异。在安慰剂试验中，PA在两组中都很明显；然而，阻塞性睡眠呼吸暂停综合征组与对照组相比，PA明显增强(最后一次低氧发作36.9+/-2.8vs.27.7+/-2.2Min-1；P<；0.01)。而阻塞性睡眠呼吸暂停综合征组vLTF明显高于对照组(29.3+/-2.8vs.20.4+/-1.3min-1，P<；0.01)。阻塞性睡眠呼吸暂停综合征患者服用抗氧化剂后，PA和vLTF较安慰剂组显著降低(PA 30.6+/-2.0vs.36.9+/-2.8vs.36.9+/-2.8P0.01；vLTF23.3+/-1.4vs.29.3+/-2.8Pt0.05)。我们的结论是，阻塞性睡眠呼吸暂停综合征患者的PA和vLTF增加，这些形式的呼吸可塑性在抗氧化剂鸡尾酒治疗后得到缓解。
Progressive augmentation (PA) and ventilatory long-term facilitation (vLTF) of respiratory motor output are forms of respiratory plasticity that are initiated during exposure to intermittent hypoxia. The present study was designed to determine whether PA and vLTF are enhanced in obstructive sleep apnoea (OSA) participants compared to matched healthy controls. The study was also designed to determine whether administration of an antioxidant cocktail mitigates PA and vLTF. Thirteen participants with sleep apnoea and 13 controls completed two trials. During both trials participants were exposed to intermittent hypoxia which included twelve 4-min episodes of hypoxia (P-ETO2, 50 mmHg; P-ETCO2, 4 mmHg above baseline) followed by 30 min of recovery. Prior to exposure to intermittent hypoxia, participants were administered, in a randomized fashion, either an antioxidant or a placebo cocktail. Baseline measures of minute ventilation during the placebo and antioxidant trials were not different between or within groups. During the placebo trial, PA was evident in both groups; however it was enhanced in the OSA group compared to control (last hypoxic episode 36.9 +/- 2.8 vs. 27.7 +/- 2.2 l min-1; P < 0.01). Likewise, vLTF was evident during the recovery period in both groups; on the other hand vLTF was greater in the OSA group compared to control (29.3 +/- 2.8 vs. 20.4 +/- 1.3 l min-1; P < 0.01). PA and vLTF were reduced in the OSA group following antioxidant administration compared to the placebo (PA 30.6 +/- 2.0 vs. 36.9 +/- 2.8 l min-1, P < 0.01; vLTF 23.3 +/- 1.4 vs. 29.3 +/- 2.8 l min-1, P < 0.05). We conclude that PA and vLTF are enhanced in participants with OSA and that these forms of respiratory plasticity are mitigated after treatment with an antioxidant cocktail.