盐酸灌注豚鼠食管诱发气道速激肽释放增加

The Role of Substance P in the Airway Neurogenic Inflammation Induced by HCl Intra-oesophageal Instillation in Guinea Pigs

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。

Objeetive The increased airway neuropeptides and neurogenic inflammation induced by HC1 intra-esophageal instillation, and the role of substance P （SP） were investigated. Methods 1N HCI （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 HC1 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 HCI 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 HC1 instillation were almost completely inhibited （P〈0.001）. Conclusion Neurogenic inflammation of airway can be induced by HC1 intra-esophageal instillation, SP plays an important role in the airway neurogenic inflammation.