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首页> 外文期刊>European journal of pain : >Central pain mechanisms following combined acid and capsaicin perfusion of the human oesophagus.
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Central pain mechanisms following combined acid and capsaicin perfusion of the human oesophagus.

机译:酸和辣椒素对人食管的联合灌注后的中枢性疼痛机制。

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Visceral afferents originating from different gut-segments converge at the spinal level. We hypothesized that chemically-induced hyperalgesia in the oesophagus could provoke widespread visceral hypersensitivity and also influence descending modulatory pain pathways. Fifteen healthy volunteers were studied at baseline, 30, 60 and 90 min after randomized perfusion of the distal oesophagus with either saline or 180 ml 0.1M HCl+2mg capsaicin. Electro-stimulation of the oesophagus, 8 cm proximal to the perfusion site, rectosigmoid electrical stimulation and rectal mechanical and heat stimulations were used. Evoked brain potentials were recorded after electrical stimulations before and after oesophageal perfusion. After the perfusion, rectal hyperalgesia to heat (P<0.01, 37%) and mechanical (P=0.01, 11%) stimulations were demonstrated. In contrast, hypoalgesia to electro-stimulation was observed in both the oesophagus (P<0.03, 23%) and the sigmoid colon (P<0.001, 18%). Referred pain areas to electro-stimulation in oesophagus were reduced by 13% after perfusion (P=0.01). Evoked brain potentials to rectosigmoid stimulations showed decreased latencies and amplitudes of P1, N1 and P2 (P<0.05), whereas oesophagus-evoked brain potentials were unaffected after perfusion. In conclusion, modality-specific hyperalgesia was demonstrated in the lower gut following chemical sensitization of the oesophagus, reflecting widespread central hyperexcitability. Conversely, hypoalgesia to electrical stimulation, decreases in referred pain and latencies of evoked brain potentials was seen. This outcome may reflect a counterbalancing activation of descending inhibitory pathways. As these findings are also seen in the clinical setting, the model may be usable for future basic and pharmacological studies.
机译:来自不同肠段的内脏传入神经在脊柱水平会聚。我们假设食道中的化学诱导的痛觉过敏可能会引起广泛的内脏超敏反应,并且还会影响下行的调节性疼痛途径。在基线,分别用盐水或180 ml 0.1M HCl + 2mg辣椒素对食管远端灌注后的30、60和90分钟,对15名健康志愿者进行了研究。使用电刺激食管(距灌注部位近8 cm),直肠乙状结肠电刺激以及直肠机械和热刺激。食管灌注前后电刺激后记录诱发的脑电势。灌注后,证实了直肠对热的痛觉过敏(P <0.01,37%)和机械刺激(P = 0.01,11%)。相反,在食道(P <0.03,23%)和乙状结肠(P <0.001,18%)中均观察到了对电刺激的痛觉过敏。灌注后,食管电刺激的疼痛区域减少了13%(P = 0.01)。直肠乙状结肠刺激引起的脑电势显示P1,N1和P2的潜伏期和振幅降低(P <0.05),而食管诱发的脑电势在灌注后不受影响。总之,在食道化学致敏后,下部肠道表现出模态特异性痛觉过敏,反映了广泛的中枢性过度兴奋性。相反,可以看到对电刺激的痛觉过敏,相应疼痛的减轻和诱发脑电势的潜伏期。这一结果可能反映了抑制途径的平衡激活。由于在临床环境中也可以看到这些发现,因此该模型可用于将来的基础和药理研究。

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