Van De Borne P, Montano N, Narkiewicz K, Degaute J P, Malliani A, Pagani M, Somers V K
Hypertension Clinic, Erasme Hospital, 1070 Brussels, Belgium.
Am J Physiol Heart Circ Physiol. 2001 Feb;280(2):H722-9. doi: 10.1152/ajpheart.2001.280.2.H722.
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, and 4) 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 CO(2) (both P < 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.
化学反射刺激会引发过度通气和交感神经激活,其中每一种对心血管变异性的振荡特征可能都有不同影响。我们在14名健康受试者中研究了过度通气对RR间期(RR)变化与肌肉交感神经活动(MSNA)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过程中对RR和MSNA变异性进行了频谱分析:1)控制呼吸,2)最大呼气末屏气,3)等碳酸血症性自主过度通气,4)高碳酸血症诱导的过度通气。MSNA在控制呼吸时为100%,在屏气时增加至170±25%(P = 0.02)。RR未改变,但RR和MSNA的标准化低频(LF)变异性均显著增加(P < 0.001)。在等碳酸血症性过度通气期间,分钟通气量增加至20.2±1.4升/分钟(P < 0.0001)。在高碳酸血症性过度通气期间,分钟通气量也增加(至19.7±1.7升/分钟),呼气末二氧化碳(两者P < 0.0001)也增加。MSNA在等碳酸血症性过度通气期间保持不变(104±7%),但在高碳酸血症性过度通气期间增加至241±49%(P < 0.01)。RR在等碳酸血症性和高碳酸血症性过度通气期间均降低(P < 0.05)。然而,尽管存在心动过速和交感神经活动增强,RR和MSNA的标准化LF变异性在等碳酸血症性和高碳酸血症性过度通气期间均降低(P < 0.05)。总之,过度通气诱导的自主神经驱动中显著的呼吸振荡可能会导致RR、MSNA和神经循环变异性之间的解离,可能是通过抑制中枢起源和/或抑制LF心血管节律的传导。