Stemper B, Hilz M J, Rauhut U, Neundörfer B
University of Erlangen Nuremberg, Department of Neurology, Germany.
Clin Auton Res. 2002 Apr;12(2):78-83. doi: 10.1007/s102860200024.
The cold face test (CFT) is a non-invasive challenge maneuver of the autonomic nervous system which activates the peripheral sympathetic and the cardiac parasympathetic nervous system and induces peripheral vasoconstriction and bradycardia. The physiology of CFT-induced bradycardia is still controversial. The heart rate decrease might result from a direct central up-regulation of cardiovagal activity or might be a secondary effect of baroreceptor activation or of changes of respiration. The purpose of this study was to analyze the origin of CFT-induced bradycardia. To evaluate the influence of respiration on bradycardia during CFT, we studied cardiac responses in 10 healthy volunteers during CFT (0-1 degrees C cold compresses for 60 s) with three different respiratory patterns: one with spontaneous and two with paced respiration (6 and 15 cycles/minute). We continuously monitored heart rate (HR), blood pressure (BP) and respiration and determined heart rate variability by assessment of coefficient of variation (CV), standard deviation (SD) and the root mean square of successive differences (RMSSD) of HR as well as low (LF) and high (HF) frequency spectra power of HR and BP. When coherence was above 0.5, we calculated the transfer function gain between HR and respiration in the HF band, as an index of respiratory sinus arrhythmia, and between HR and BP in the LF band, as an index of baroreflex sensitivity. HR decreased and BP increased significantly during the three types of CFT. The decrease of HR and the increase of BP, of time and frequency domain parameters did not differ between the three breathing patterns. Respiration, and HF and LF power of respiration did not change during CFT. The gain of the HF-transfer function between HR and respiration and the LF-transfer function gain between HR and BP increased significantly during CFT, but the increase did not differ between the three breathing patterns. The increase of the gain of both transfer functions is most likely due to an increase of vagal traffic and together with the unchanged respiratory pattern suggests that CFT-induced bradycardia is not due to baroreflex or respiratory influences, but seems to result from central vagal activation.
冷脸试验(CFT)是一种自主神经系统的非侵入性激发操作,可激活外周交感神经和心脏副交感神经系统,并诱发外周血管收缩和心动过缓。CFT诱发心动过缓的生理机制仍存在争议。心率下降可能是由于心血管迷走神经活动的直接中枢上调,也可能是压力感受器激活或呼吸变化的继发效应。本研究的目的是分析CFT诱发心动过缓的起源。为了评估呼吸对CFT期间心动过缓的影响,我们研究了10名健康志愿者在CFT(0-1摄氏度冷敷60秒)期间的心脏反应,采用三种不同的呼吸模式:一种是自发呼吸,另外两种是定频呼吸(6次和15次/分钟)。我们持续监测心率(HR)、血压(BP)和呼吸,并通过评估HR的变异系数(CV)、标准差(SD)和逐次差值的均方根(RMSSD)以及HR和BP的低频(LF)和高频(HF)频谱功率来确定心率变异性。当相干性高于0.5时,我们计算HF频段HR与呼吸之间的传递函数增益,作为呼吸性窦性心律不齐的指标,以及LF频段HR与BP之间的传递函数增益,作为压力反射敏感性的指标。在三种类型的CFT期间,HR显著下降,BP显著升高。三种呼吸模式之间,HR下降、BP升高以及时域和频域参数的变化并无差异。CFT期间呼吸以及呼吸的HF和LF功率未发生变化。HR与呼吸之间HF传递函数的增益以及HR与BP之间LF传递函数的增益在CFT期间显著增加,但三种呼吸模式之间的增加并无差异。两种传递函数增益的增加很可能是由于迷走神经活动增加,并且与不变的呼吸模式一起表明,CFT诱发的心动过缓并非由于压力反射或呼吸影响,而是似乎源于中枢迷走神经激活。