Hollerbach S, Bulat R, May A, Kamath M V, Upton A R, Fallen E L, Tougas G
Department of Medicine, Division of Gastroenterology, Mcmaster University, Hamilton, Ontario, Canada.
Neurogastroenterol Motil. 2000 Dec;12(6):555-65. doi: 10.1046/j.1365-2982.2000.00230.x.
In noncardiac chest pain (NCCP), altered visceral perception may result from abnormal cerebral processing of sensory input rather than abnormalities of afferent pathways. However, the interactions between symptoms, autonomic function and oesophageal stimuli are poorly studied. Oesophageal stimulation elicits reproducible cortical evoked potentials [CEP] and modulates heart rate variability via vagal pathways, as visible on power spectrum analysis of heart rate variability [PS-HRV]. These methods are increasingly used to study the function of visceral afferent neural pathways in human. The aim of this study was to compare EP and PS-HRV during oesophageal stimuli in NCCP and controls. Twelve healthy volunteers (one female, 11 male; aged 24-51 years; mean 32 +/- 8 years), and eight NCCP patients (three female, five male; age range 26-58, mean 40.5 +/- 10 years) were studied. Electrical oesophageal stimulation (EOS; 200 microseconds, 0.2 Hz, 25 stimuli) was applied to the oesophageal wall 5 cm above the lower oesophageal sphincter (LOS), and perception thresholds (measured in mA) determined. EP responses were recorded using 22 standard electroencephalogram scalp electrodes. Autonomic activity was assessed using PS-HRV, before, during, and after oesophageal stimulation. Measured PS-HRV indices included high frequency (HF; 0. 15-0.5 Hz) and low frequency (LF; 0.06-0.15 Hz) power, respectively, assessing vagal and sympathetic activity, and the LF/HF ratio. EOS perception occurred at lower thresholds in NCCP than in controls (3. 6 +/- 1 vs. 7.8 +/- 2 mA, P < 0.05). EP amplitude was greater (13 +/- 2 vs. 6 +/- 1 microV, P < 0.0001), and latency longer in controls vs. NCCP (191 +/- 7 ms vs. 219 +/- 6 ms, P < 0.001). In NCCP, EOS decreased sympathetic outflow (low frequency peak on PS-HRV) and increased cardiovagal activity (high frequency peak, P < 0.02) to a significantly higher degree in comparison with controls. During EOS, heart rate decreased in NCCP from 68 vs. 62 beats min-1 (P < 0.003) but not in controls. In NCCP patients, EOS was perceived at lower intensities and was associated with a greater cardiovagal reflex response. EP responses associated with EOS were smaller in NCCP than in controls, suggesting that an increased perception of oesophageal stimuli results from an enhanced cerebral processing of visceral sensory input in NCCP, rather than from hyperalgesic responses in visceral afferent pathways.
在非心源性胸痛（NCCP）中，内脏感觉改变可能是由于大脑对感觉输入的异常处理，而非传入通路的异常。然而，症状、自主神经功能和食管刺激之间的相互作用研究较少。食管刺激可诱发可重复的皮层诱发电位[CEP]，并通过迷走神经通路调节心率变异性，这在心率变异性功率谱分析[PS-HRV]中可见。这些方法越来越多地用于研究人类内脏传入神经通路的功能。本研究的目的是比较NCCP患者和对照组在食管刺激期间的诱发电位（EP）和PS-HRV。研究了12名健康志愿者（1名女性，11名男性；年龄24 - 51岁；平均32±8岁）和8名NCCP患者（3名女性，5名男性；年龄范围26 - 58岁，平均40.5±10岁）。在食管下括约肌（LOS）上方5 cm处的食管壁施加电食管刺激（EOS；200微秒，0.2 Hz，25次刺激），并确定感觉阈值（以毫安为单位测量）。使用22个标准脑电图头皮电极记录EP反应。在食管刺激前、期间和之后，使用PS-HRV评估自主神经活动。测量的PS-HRV指标包括高频（HF；0.15 - 0.5 Hz）和低频（LF；0.06 - 0.15 Hz）功率，分别评估迷走神经和交感神经活动，以及LF/HF比值。NCCP患者的EOS感觉阈值低于对照组（3.6±1 vs. 7.8±2 mA，P < 0.05）。对照组的EP波幅更大（13±2 vs. 6±1微伏，P < 0.0001），潜伏期更长（191±7毫秒 vs. 219±6毫秒，P < 0.001）。与对照组相比，在NCCP中，EOS使交感神经输出减少（PS-HRV上的低频峰值），并使心脏迷走神经活动增加（高频峰值，P < 0.02），程度显著更高。在EOS期间，NCCP患者的心率从68次/分钟降至62次/分钟（P < 0.003），而对照组未下降。在NCCP患者中，EOS在较低强度时即可被感知，并与更大的心脏迷走神经反射反应相关。与对照组相比，NCCP患者中与EOS相关的EP反应较小，这表明NCCP中食管刺激感觉增强是由于大脑对内脏感觉输入的处理增强，而非内脏传入通路的痛觉过敏反应。
