Importance of ventilation in modulating interaction between sympathetic drive and cardiovascular variability.
Importance of ventilation in modulating interaction between sympathetic drive and cardiovascular variability.
复制标题
通气在调节交感神经驱动和心血管变异之间的相互作用中的重要性。
DOI：
10.1152/ajpheart.2001.280.2.h722
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Somers,VK
中科院分区：
文献类型：
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作者：
VanDeBorne,P;Montano,N;Narkiewicz,K;Degaute,JP;Malliani,A;Pagani,M;Somers,VK
化学反射刺激引起过度通气和交感神经激活，每一种都可能对心血管变异性的振荡特性产生不同的影响。在14名健康受试者中，我们研究了过度通气对R-R间期（RR）和肌肉交感神经活动（MSNA）变化之间的相互作用以及神经循环变异性变化的影响。我们在以下每种干预措施中对RR和MSNA变异性进行频谱分析：1）控制呼吸，2）最大呼气末呼吸暂停，3）等二氧化碳自主过度通气，4）高碳酸血症诱导的过度通气。MSNA从控制呼吸期间的100%增加到呼吸暂停期间的170 ± 25%（P = 0.02）。RR无变化，但RR和MSNA的标准化低频（LF）变异性显著增加（P <0.001）。在等二氧化碳过度通气期间，每分钟通气量增加至20.2 ± 1.4 l/min（P <0.0001）。在高碳酸血症过度通气时，每分钟通气量也增加（至19.7 ± 1.7 l/min），潮气末CO2也增加（均P <0.0001）。MSNA在等二氧化碳过度通气时无变化（104 ± 7%），但在高二氧化碳过度通气时增加到241 ± 49%（P <0.01）。等碳酸和高碳酸过度通气时RR均降低（P <0.05）。然而，在等碳酸血症和高碳酸血症过度通气期间，尽管存在心动过速和交感神经交通增加，RR和MSNA的标准化LF变异性降低（P <0.05）。总之，过度通气引起的自主驱动中显著的呼吸振荡可能会诱导RR、MSNA和神经循环变异性之间的分离，这可能是通过抑制中枢发生和/或抑制LF心血管节律的传递。
Chemoreflex stimulation elicits both hyperventilation and sympathetic activation, each of which may have different influences on oscillatory characteristics of cardiovascular variability. We examined the influence of hyperventilation on the interactions between changes in R-R interval (RR) and muscle sympathetic nerve activity (MSNA) and changes in neurocirculatory variability, in 14 healthy subjects. We performed spectral analysis of RR and MSNA variability during each of the following interventions:1)controlled breathing,2)maximal end-expiratory apnea,3)isocapnic voluntary hyperventilation, and4)hypercapnia-induced hyperventilation. MSNA increased from 100% during controlled breathing to 170 ± 25% during apnea (P= 0.02). RR was unchanged, but normalized low-frequency (LF) variability of both RR and MSNA increased markedly (P< 0.001). During isocapnic hyperventilation, minute ventilation increased to 20.2 ± 1.4 l/min (P< 0.0001). During hypercapnic hyperventilation, minute ventilation also increased (to 19.7 ± 1.7 l/min) as did end-tidal CO2(bothP< 0.0001). MSNA remained unchanged during isocapnic hyperventilation (104 ± 7%) but increased to 241 ± 49% during hypercapnic hyperventilation (P< 0.01). RR decreased during both isocapnic and hypercapnic hyperventilation (P< 0.05). However, normalized LF variability of RR and of MSNA decreased (P< 0.05) during both isocapnic and hypercapnic hyperventilation, despite the tachycardia and heightened sympathetic nerve traffic. In conclusion, marked respiratory oscillations in autonomic drive induced by hyperventilation may induce dissociation between RR, MSNA, and neurocirculatory variability, perhaps by suppressing central genesis and/or inhibiting transmission of LF cardiovascular rhythms.