The need for specificity in quantifying neurocirculatory vs. respiratory effects of eucapnic hypoxia and transient hyperoxia.
The need for specificity in quantifying neurocirculatory vs. respiratory effects of eucapnic hypoxia and transient hyperoxia.
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在量化欧研究生缺氧和瞬时高氧的神经循环与呼吸作用方面的特异性需求。
DOI：
10.1113/jp280515
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发表时间：
2020-11
期刊：
影响因子：
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通讯作者：
Dempsey JA
中科院分区：
文献类型：
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作者：
Prasad B;Morgan BJ;Gupta A;Pegelow DF;Teodorescu M;Dopp JM;Dempsey JA
颈动脉化学感受器的超敏性导致交感神经系统激活和呼吸不稳定，这与几种常见临床病症的发病机制和后果有关。目前正在研究各种旨在减轻化学感受器驱动的交感神经过度活跃的治疗方法;因此，以特异性和精确度量化该结果变量的能力至关重要。因此，我们测量了持续气道正压通气治疗阻塞性睡眠呼吸暂停的中年男性和女性（n=82）对短暂高氧和化学反射兴奋引起的化学反射抑制的呼吸和神经循环反应。进行性、正常二氧化碳性缺氧导致通气量（+83 59%）和肌肉交感神经活动（MSNA）爆发频率（+55 31%）显著增加，而短暂性高氧导致这些变量显著减少（分别为-35 ±14%和-42 ± 16%）。变异系数的解释和MSNA爆发频率响应，表明重测重现性，分别为9%和24%，高氧和35%和28%，缺氧。基于等级相关性的统计测量，甚至在四分位数的相应的抑制和MSNA响应的比较，我们发现，高氧或兴奋与eucapnic缺氧的抑制的幅度与相应的MSNA响应在个人内不相关。我们的结论是，在有意识的，行为的人，渐进的，稳态的，eucapnic缺氧和短暂的高氧的解释敏感性不预测MSNA的反应。我们的研究结果也支持使用短暂的高氧作为一个可靠的，敏感的，测量颈动脉化学感受器的贡献，紧张性交感神经系统的活动和呼吸驱动。
Hypersensitivity of the carotid chemoreceptor leading to sympathetic nervous system activation and ventilatory instability has been implicated in the pathogenesis and consequences of several common clinical conditions. A variety of treatment approaches aimed at lessening chemoreceptor-driven sympathetic overactivity is now under investigation; thus, the ability to quantify this outcome variable with specificity and precision is crucial. Accordingly, we measured ventilatory and neurocirculatory responses to chemoreflex inhibition elicited by transient hyperoxia and chemoreflex excitation produced by exposure to graded, steady-state eucapnic hypoxia in middle-aged men and women (n=82) with continuous positive airway pressure-treated obstructive sleep apnea. Progressive, eucapnic hypoxia produced robust and highly variable increases in ventilation (+83±59%) and muscle sympathetic nerve activity (MSNA) burst frequency (+55±31%), whereas transient hyperoxia caused marked reductions in these variables (−35±14% and −42±16%, respectively). Coefficients of variation for ventilatory and MSNA burst frequency responses, indicating test-retest reproducibility, were 9% and 24% for hyperoxia and 35% and 28% for hypoxia. Based on statistical measures of rank correlation or even comparisons across quartiles of corresponding ventilatory and MSNA responses, we found that the magnitudes of ventilatory inhibition with hyperoxia or excitation with eucapnic hypoxia were not correlated with corresponding MSNA responses within individuals. We conclude that, in conscious, behaving humans, ventilatory sensitivities to progressive, steady-state, eucapnic hypoxia and transient hyperoxia do not predict MSNA responsiveness. Our findings also support the use of transient hyperoxia as a reliable, sensitive, measure of the carotid chemoreceptor contribution to tonic sympathetic nervous system activity and respiratory drive.