Intraesophageal chemicals enhance responsiveness of upper thoracic spinal neurons to mechanical stimulation of esophagus in rats.
Intraesophageal chemicals enhance responsiveness of upper thoracic spinal neurons to mechanical stimulation of esophagus in rats.
复制标题
食管内化学物质增强大鼠上胸椎神经元对食管机械刺激的反应性。
DOI：
10.1152/ajpgi.00477.2007
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Foreman,RobertD
中科院分区：
文献类型：
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作者：
Qin,Chao;Farber,JayP;Foreman,RobertD
食管过敏是患者非心源性胸痛的最常见原因之一。在这项研究中，我们调查是否暴露的食管酸和其他化学刺激物的影响活动的胸脊髓神经元响应食管扩张（艾德）在大鼠。在戊巴比妥钠麻醉、麻痹和通气的雄性大鼠中记录单个胸（T3）脊髓神经元的细胞外电位。通过将乳胶球囊经口放入食道中胸区域，用水充气产生艾德（0.2或0.4 ml，20 s）。通过一根穿过胃并放置在胸食管中的管子给予化学品。为了刺激食管，注射0.2 ml HCl（0.01 N）、缓激肽（10 μg/ml）或辣椒素（10 μ g/ml）1-2 min。本研究仅包括由艾德兴奋的神经元。结果显示，食管内灌注盐酸、缓激肽和辣椒素分别增加了3/20（15%）、7/25（28%）和9/20（45%）神经元的活性，但增强了其余脊髓神经元中9/17（53%）、8/15（53%）和7/11（64%）对艾德的兴奋反应。此外，食管内化学物质更可能提高低阈值神经元比高阈值神经元对食管机械刺激的反应性。生理盐水（pH 7.4，0.2 ml）或溶剂滴入食管没有显着影响的活动或艾德反应的神经元。我们的结论是，胸脊髓神经元增强反应艾德的化学挑战食管可能提供了一个可能的病理生理基础内脏高敏感性患者胃食管反流和/或食管炎。
Esophageal hypersensitivity is one of the most common causes of noncardiac chest pain in patients. In this study, we investigated whether exposure of the esophagus to acid and other chemical irritants affected activity of thoracic spinal neurons responding to esophageal distension (ED) in rats. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital sodium-anesthetized, -paralyzed, and -ventilated male rats. ED (0.2 or 0.4 ml, 20 s) was produced by water inflation of a latex balloon placed orally into the middle thoracic region of the esophagus. The chemicals were administered via a tube that was passed through the stomach and placed in the thoracic esophagus. To irritate the esophagus, 0.2 ml of HCl (0.01 N), bradykinin (10 μg/ml), or capsaicin (10 μg/ml) were injected for 1–2 min. Only neurons excited by ED were included in this study. Results showed that intraesophageal instillation of HCl, bradykinin, and capsaicin increased activity in 3/20 (15%), 7/25 (28%), and 9/20 (45%) neurons but enhanced excitatory responses to ED in 9/17 (53%), 8/15 (53%), and 7/11 (64%) of the remaining spinal neurons, respectively. Furthermore, intraesophageal chemicals were more likely to enhance the responsiveness of low-threshold neurons than high-threshold neurons to the esophageal mechanical stimulus. Normal saline (pH 7.4, 0.2 ml) or vehicle instilled in the esophagus did not significantly affect activity or ED responses of neurons. We conclude that enhanced responses of thoracic spinal neurons to ED by the chemically challenged esophagus may provide a possible pathophysiological basis for visceral hypersensitivity in patients with gastroesophageal reflux and/or esophagitis.