摘要
目的观察迷走神经在盐酸灌注食管引起的气道神经源性炎症中的作用。方法给麻醉豚鼠食管灌注1mol/L盐酸,观察气管、主支气管、细支气管的微血管血浆渗出和P物质(SP)、降钙素基因相关肽(CGRP)的变化,及神经内肽酶抑制剂phosphoramidon、预先切断豚鼠双侧迷走神经对上述指标的影响。气道血浆渗出采用伊文思蓝法检测,气管组织匀浆SP测定采用ELISA法,CGRP测定采用放射免疫法。结果盐酸灌注豚鼠食管显著增加气管、主支气管的SP浓度及血浆渗出(P<0.01),而细支气管的血浆渗出和SP浓度增加不明显(P>0.05);神经内肽酶抑制剂phosphoramidon可以显著增加盐酸灌注食管引起的气管、主支气管、细支气管血浆渗出(P<0.001);切断豚鼠双侧迷走神经,盐酸灌注食管诱发的气管、主支气管、细支气管SP水平增加和血浆渗出能被明显抑制(P<0.01)。结论迷走神经在盐酸灌注食管诱导的气道神经源性炎症中起着重要作用。
Objective To observe the neurogenic inflammation induced by HC1 intra- oesophageal instillation, and the role of bilaterally vagus nerve vagotomized. Methods Infusion of 1 N HCl into the esophagus of anesthetized guinea pigs, the microvascular leakage was examined in the presence or absence of neutral endopeptidase inhibitor phosphoramidon and bilaterally vagus nerve vagotomized. The airway plasma leakage was evaluated by measuring extravasated Evans blue dye. SP concentration was measured with Enzyme -Linked Immunosorbent Assay （ELISA） ; and CGRP was measured by radioimmunoassay （KIA）. Results Infusion of 1 mol/L HC1 into the esophagus significantly increased the tracheal and mainstem bronchial SP level and Evans blue dye concentration （P 〈0. 01 ）, but no significantly increased in bronchiolies （P 〉 0.05 ）. Phosphoramidon significantly potentiated SP level and Evans blue dye concentration in the trachea, main bronchi and bronchial （P 〈 0. 001 ）. Airway plasma extravasation and the increased SP level induced by intra - esophageal HCl instillation were also significantly inhibited by bilateral vagotomy （P 〈 0.01 ）. Conclusion Intra - esophageal acid stimulation can induce airway neurogenic inflammation, and vagus nerve plays an important role in it.
出处
《广东医学》
CAS
CSCD
北大核心
2007年第7期1027-1029,共3页
Guangdong Medical Journal
基金
国家自然科学基金资助项目(编号:30370621)
教育部科学技术重点项目(编号:205117)
广州医学院博士启动项目(编号:2006066)
作者简介
通讯作者，E—mail：klai@163．net
