Ponikowski P, Chua T P, Piepoli M, Ondusova D, Webb-Peploe K, Harrington D, Anker S D, Volterrani M, Colombo R, Mazzuero G, Giordano A, Coats A J
Department of Cardiac Medicine, Imperial College School of Medicine, National Heart and Lung Institute, London, UK.
Circulation. 1997 Oct 21;96(8):2586-94. doi: 10.1161/01.cir.96.8.2586.
The precise mechanisms responsible for the sympathetic overactivity and blunted baroreflex control in chronic heart failure (CHF) remain obscure. Augmented peripheral chemosensitivity has recently been demonstrated in CHF. We evaluated the relation between peripheral chemoreflex sensitivity and autonomic activity in patients with CHF.
We studied in 26 stable patients with CHF the peripheral chemosensitivity (ventilatory response to hypoxia using transient inhalations of pure nitrogen), autonomic balance (spectral analysis of heart rate variability [HRV]), and baroreflex sensitivity (bolus phenylephrine method and alpha index). To determine whether transient inactivation of peripheral chemoreceptors might influence autonomic balance, 12 patients underwent a second study during which they breathed 100% O2. Peripheral chemosensitivity correlated inversely with HRV power within the low-frequency band (0.04 to 0.15 Hz) (r=-.52, P=.006) and inversely with baroreflex sensitivity (r=-.60, P=.005). When the patients were divided into two groups according to the chemosensitivity of age-matched normal controls (above and below mean+2 SDs of chemosensitivity of control subjects), those above the normal range revealed more impaired autonomic balance, ie, lower baroreflex sensitivity (1.4 +/- 1.3 versus 5.0 +/- 1.5 ms/mm Hg, P<.0001) and depressed values of low-frequency power (2.5 +/- 1.8 versus 4.1 +/- 0.8 ln ms2, P<.005) compared with those with normal chemosensitivity. Transient hyperoxia did not alter heart rate or systolic pressure but resulted in an increase in HRV and an improvement in baroreflex sensitivity.
A link between increased peripheral chemosensitivity and impaired autonomic control, including baroreflex inhibition, is demonstrated. The clinical importance of this phenomenon warrants further investigation.
慢性心力衰竭（CHF）中交感神经过度活跃和压力反射控制减弱的确切机制仍不清楚。最近已证实在CHF中存在外周化学敏感性增强。我们评估了CHF患者外周化学反射敏感性与自主神经活动之间的关系。
我们研究了26例稳定的CHF患者的外周化学敏感性（通过短暂吸入纯氮对低氧的通气反应）、自主神经平衡（心率变异性[HRV]的频谱分析）和压力反射敏感性（苯肾上腺素推注法和α指数）。为了确定外周化学感受器的短暂失活是否会影响自主神经平衡，12例患者进行了第二项研究，期间他们吸入100%氧气。外周化学敏感性与低频带（0.04至0.15Hz）内的HRV功率呈负相关（r = -0.52，P = 0.006），与压力反射敏感性呈负相关（r = -0.60，P = 0.005）。当根据年龄匹配的正常对照的化学敏感性（高于和低于对照受试者化学敏感性的均值+2个标准差）将患者分为两组时，高于正常范围的患者显示出更受损的自主神经平衡，即与化学敏感性正常的患者相比，压力反射敏感性更低（1.4±1.3对5.0±1.5ms/mm Hg，P<0.0001），低频功率值降低（2.5±1.8对4.1±0.8ln ms2，P<0.005）。短暂性高氧并未改变心率或收缩压，但导致HRV增加和压力反射敏感性改善。
证实了外周化学敏感性增加与自主神经控制受损（包括压力反射抑制）之间的联系。这一现象的临床重要性值得进一步研究。
