Daytime loop gain is elevated in obstructive sleep apnea but not reduced by CPAP treatment.
Daytime loop gain is elevated in obstructive sleep apnea but not reduced by CPAP treatment.
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阻塞性睡眠呼吸暂停患者的日间循环增益会升高，但 CPAP 治疗不会降低白天循环增益。
DOI：
10.1152/japplphysiol.00175.2018
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Catcheside,PeterG
中科院分区：
文献类型：
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作者：
Deacon-Diaz,NaomiLouise;Sands,ScottA;McEvoy,RDoug;Catcheside,PeterG
呼吸控制稳定性降低（环路增益升高）是导致阻塞性睡眠呼吸暂停（OSA）的关键非解剖学病理学特征，但其机制尚不清楚。我们试图确定导致OSA环路增益升高的关键因素（控制器与植物贡献），并检查这些因素的异常是否在OSA治疗后持续存在。在15名男性（8名OSA，7名身高、体重和年龄匹配的对照）中，我们在清醒期间使用伪随机二进制CO2刺激方法测量回路增益、控制器增益和植物增益。还评估了潜在影响植物增益的因素（通过氦气稀释和肺活量测定法测定仰卧位肺容量）。在开始持续气道正压通气治疗后2周和6周重复测量。OSA组的环路增益（LG）高于对照组（LG在1次循环/min时分别为0.28 ± 0.04vs.0.16 ± 0.04，P = 0.046），OSA组的控制器对CO2的峰值响应更大，滚降更快。与对照组相比，OSA患者还表现出第一秒用力呼气量和用力肺活量减少（分别为92.2 ± 1.7 vs. 102.9 ± 3.5%预测值，P= 0.021; 93.4 ± 3.1 vs. 106.6 ± 3.6%预测值，P= 0.015）。给药对任何变量均无影响。这些研究结果证实，未经治疗的OSA患者的环路增益高于匹配的对照组;然而，这并不受治疗的影响。新&值得注意的是，环路增益升高有助于阻塞性睡眠呼吸暂停（OSA）的病理生理学。然而，回路增益是否在OSA中固有地升高或由OSA本身诱导，它是否由于化学反射敏感性增加或肥胖依赖性肺容量减少而升高，以及它是否是治疗可逆的，目前都是不确定的。这项研究发现，与年龄、性别、身高和体重匹配的对照组相比，OSA患者的环路增益升高。然而，这并没有改变6周的持续气道正压通气治疗。
Reduced ventilatory control stability (elevated loop gain) is a key nonanatomical, pathological trait contributing to obstructive sleep apnea (OSA), yet the mechanisms responsible remain unclear. We sought to identify the key factors contributing to elevated loop gain in OSA (controller vs. plant contributions) and to examine whether abnormalities in these factors persist after OSA treatment. In 15 males (8 OSA, 7 height, weight- and age -matched controls), we measured loop gain, controller gain, and plant gain using a pseudorandom binary CO2stimulation method during wakefulness. Factors potentially influencing plant gain were also assessed (supine lung volume via helium dilution and spirometry). Measures were repeated 2 and 6 wk after initiating continuous positive airway pressure treatment. Loop gain (LG) was higher in OSA versus controls (LG at 1 cycle/min 0.28 ± 0.04 vs. 0.16 ± 0.04,P= 0.046, respectively), and the controller exhibited a greater peak response to CO2and faster roll-off in OSA. OSA patients also exhibited reduced forced expiratory volume in the first second and forced vital capacity compared with controls (92.2 ± 1.7 vs. 102.9 ± 3.5% predicted,P= 0.021; 93.4 ± 3.1 vs. 106.6 ± 3.6% predicted,P= 0.015, respectively). There was no effect of treatment on any variable. These findings confirm loop gain is higher in untreated OSA patients than in matched controls; however, this was not affected by treatment.NEW & NOTEWORTHYElevated loop gain contributes to obstructive sleep apnea (OSA) pathophysiology. However, whether loop gain is inherently elevated in OSA or induced by OSA itself, whether it is elevated due to increased chemoreflex sensitivity or obesity-dependent reduced lung volume, and whether it is treatment reversible, are all currently uncertain. This study found loop gain was elevated in OSA versus age-, sex-, height-, and weight-matched controls. However, this was not altered by 6-wk continuous positive airway pressure treatment.