CAJ | 학술논문

目的本研究旨在观察盐酸灌注食管是否可以引起速激肽释放及气道神经源性炎症。方法给麻醉豚鼠食管下段灌注1N 盐酸（0.4mL），观察气道 P 物质（SP）、降钙素基因相关肽（CGRP）的变化，SP 测定采用酶免法，CGRP 测定采用放射免疫法。结果盐酸灌注豚鼠食管明显增加气管、主支气管的 SP 含量（P ＜0.01）；预先给予 SP 受体拮抗剂 SR140333，盐酸灌注食管诱发的气道 SP 增加能被明显抑制（P ＜0.01）。用辣椒素耗竭速激肽后，酸灌注食管诱发的气道 SP 释放几乎被完全抑制（P ＜0.001）。结论盐酸灌注食管可以引起气道神经源性炎症，SP 在盐酸灌注食管诱导的神经源性炎症中起重要作用。
목적본연구지재관찰염산관주식관시부가이인기속격태석방급기도신경원성염증。방법급마취돈서식관하단관주1N 염산（0.4mL），관찰기도 P 물질（SP）、강개소기인상관태（CGRP）적변화，SP 측정채용매면법，CGRP 측정채용방사면역법。결과염산관주돈서식관명현증가기관、주지기관적 SP 함량（P ＜0.01）；예선급여 SP 수체길항제 SR140333，염산관주식관유발적기도 SP 증가능피명현억제（P ＜0.01）。용랄초소모갈속격태후，산관주식관유발적기도 SP 석방궤호피완전억제（P ＜0.001）。결론염산관주식관가이인기기도신경원성염증，SP 재염산관주식관유도적신경원성염증중기중요작용。
Objective The increased airway neuropeptides and neurogenic inflammation induced by HCl intra-esophageal instillation, and the role of substance P (SP) were investigated. Methods 1N HCl (0.4mL) was infused into the esophagus of anesthetized guinea pigs, the substance P (SP) and CGRP level in airway were examined by ELISA and by radioimmunoassay, respectively. Results Infusion of 1N HCl into the esophagus significantly increased the tracheal and mainstem bronchial SP level (P<0.01). Phosphoramidon significantly potentiated SP level (P<0.001). Airway plasma extravasation and the increased SP level induced by intra-esophageal HCl instillation were also significantly inhibited by pretreatment of SR140333 (P<0.01). After capsaicin pretreatment to exhaust the systemic tachykinins, the increased SP level induced by intra-esophageal HCl instillation were almost completely inhibited (P<0.001). Conclusion Neurogenic inflammation of airway can be induced by HCl intra-esophageal instillation, SP plays an important role in the airway neurogenic inflammation.