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人类心率和血压变异性的生理学与病理生理学:功率谱分析在很大程度上是压力反射增益的指标吗?

Physiology and pathophysiology of heart rate and blood pressure variability in humans: is power spectral analysis largely an index of baroreflex gain?

作者信息

Sleight P, La Rovere M T, Mortara A, Pinna G, Maestri R, Leuzzi S, Bianchini B, Tavazzi L, Bernardi L

机构信息

Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, U.K.

出版信息

Clin Sci (Lond). 1995 Jan;88(1):103-9. doi: 10.1042/cs0880103.

Abstract
  1. It is often assumed that the power in the low- (around 0.10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects sympathetic and vagal tone [corrected] respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Boer model). 2. We have applied the De Boer model of circulatory variability to patients with varying baroreflex sensitivity to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2 Hz), which were both distinct from the controlled respiration rate (0.25 Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Boer model. The low-frequency (0.1 Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 人们通常认为,通过对心血管变量进行功率谱分析得到的低频(约0.10赫兹)和高频(约0.25赫兹)频段的功率分别反映交感神经和迷走神经张力[已修正]。另一种模型将低频段归因于控制系统中的一种共振,这种共振是由压力反射(德布尔模型)的交感神经(有或无副交感神经)臂对逐搏血压变化的反射反应的低效缓慢时间常数产生的。2. 我们已将循环变异性的德布尔模型应用于压力反射敏感性不同的患者以及一名正常受试者,结果表明,受试者之间和受试者内部频谱功率(低频和高频)的主要差异是由动脉压力反射增益的变化引起的,特别是对于迷走神经对心率(R-R间期)和左心室搏出量的控制。我们计算了静息状态和颈部吸引(刺激颈动脉压力感受器)期间的功率谱。在正常受试者和压力反射控制敏感或较差的心力衰竭患者中,我们以两种不同于受控呼吸频率(0.25赫兹)的频率(0.1和0.2赫兹)刺激压力感受器。3. 数据大致证实了德布尔模型。只有当自主神经输出的压力反射控制相对完整时,R-R或血压变异性中的低频(0.1赫兹)峰值才会自发产生。(摘要截选至250字)

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