Department of Gastroenterology and Hepatology, St George Hospital and University of NSW, Sydney, NSW, Australia.
Clin J Pain. 2013 Jan;29(1):70-7. doi: 10.1097/AJP.0b013e3182478826.
Sensitization of esophageal chemoreceptors, either directly by intermittent acid exposure or indirectly through esophagitis-associated inflammatory mediators, is likely to be the mechanism underlying the perception of heartburn.
To compare basal esophageal sensitivity with electrical stimulation and acid, and to compare the degree of acid-induced sensitization in controls and in patient groups across the entire spectrum of gastroesophageal reflux disease: erosive oesophagitis (EO), nonerosive reflux disease (NERD), and functional heartburn (FH).
Esophageal sensory and pain thresholds to electrical stimulation were measured before, 30, and 60 minutes after an intraesophageal infusion of saline or HCl. Patients received a 30-minute infusion of 0.15 M HCl and controls were randomized to receive either HCl (n = 11) or saline (n = 10). After electrical sensory threshold testing, participants received another 30-minute infusion of HCl to determine whether sensitivity to acid is increased by prior acid exposure
All patient groups had higher basal sensory thresholds than healthy controls (controls, 13 ± 1.4 mA; FH, 20 ± 5.1 mA; NERD, 21 ± 5.1 mA; EO, 23 ± 5.4 mA; P < 0.05). Acute esophageal acid exposure reduced sensory thresholds to electrical stimulation in FH and NERD patients (P < 0.05). The level of acid sensitivity during the first HCl infusion was comparable between all patient groups and controls. The secondary infusion caused increased discomfort in all participants (P < 0.01). This acid-induced sensitization to HCl was significantly elevated in the patient groups ( P < 0.05).
(1) Esophageal acid infusion sensitizes it to subsequent electrical and chemical stimulation. (2) The acid-related sensitization is greater in gastroesophageal reflux disease than in controls and may influence in part symptom perception in this population. (3) Acid-related sensitization within the gastroesophageal reflux disease population is not dependant on mucosal inflammation.
食管化学感受器的敏化，无论是通过间歇性酸暴露直接引起，还是通过食管炎相关的炎症介质间接引起，都可能是引起烧心感的机制。
比较基础食管敏感性与电刺激和酸的关系，并比较整个胃食管反流病（GERD）谱中的对照组和患者组的酸诱导敏感性程度：糜烂性食管炎（EO）、非糜烂性反流病（NERD）和功能性烧心（FH）。
在食管内输注生理盐水或 HCl 前后 30 分钟和 60 分钟测量食管感觉和疼痛阈值。患者接受 30 分钟 0.15 M HCl 输注，对照组随机接受 HCl（n = 11）或生理盐水（n = 10）输注。在电感觉阈值测试后，参与者接受另一个 30 分钟 HCl 输注，以确定先前酸暴露是否会增加对酸的敏感性。
所有患者组的基础感觉阈值均高于健康对照组（对照组，13 ± 1.4 mA；FH 组，20 ± 5.1 mA；NERD 组，21 ± 5.1 mA；EO 组，23 ± 5.4 mA；P < 0.05）。急性食管酸暴露降低了 FH 和 NERD 患者的电刺激感觉阈值（P < 0.05）。在所有患者组和对照组之间，第一次 HCl 输注期间的酸敏感性水平相当。第二次输注引起所有参与者的不适增加（P < 0.01）。所有患者组的这种酸诱导的 HCl 敏化均显著升高（P < 0.05）。
（1）食管酸输注使食管对随后的电刺激和化学刺激敏感。（2）与对照组相比，GERD 患者的酸相关敏化更严重，这可能部分影响该人群的症状感知。（3）GERD 人群中与酸相关的敏化与黏膜炎症无关。
