摘要
目的观察热及酸刺激豚鼠食管对气道的影响，探讨瞬时受体电位香草酸亚型1（TRPV1）及神经肽在发生机制中的作用。方法构建豚鼠食管灌流模型，进行持续（20min）热生理盐水（45℃）和盐酸（0．1mol／L，37℃）灌流刺激食管，通过伊文思蓝染色法检测其气管、支气管及细支气管的血浆渗出，观察支气管肺泡灌洗液中炎症细胞总数及分类，并观察TRPV1特异性受体拮抗剂CPZ和神经内肽酶抑制剂磷阿米酮对刺激效应的影响。结果与对照组相比（P值均〈0．05），热刺激和酸刺激豚鼠食管均可增加其气管、支气管和细支气管血浆渗出；CPZ能抑制热和盐酸刺激引起的气管、支气管血浆渗出增多（P值均〈0．05）；磷阿米酮能明显增强盐酸和热刺激的效果（P值均〈0．05）。结论热、酸刺激豚鼠食管会引起气道血浆渗出增多，TRPVI及神经肽可能参与其发生机制。
Objective To observe the effect on airway of hot and acid factor stimulated in guinea pigs esophagus,as well as to investigate the mechanism of transient receptor potential vanilloid 1 （TRPV1） and neuropeptide in this process. Methods The esophagus of guinea pigs were perfused with hot saline（45℃） and hydrochloric acid （0.1 mol/L, 37 ℃） pretreatment or without TRPV1 antagonist capsazepine and inhibitor of neutral endopeptidase phosphoramidone. The microvascular leakage of trachea,main bronchi and bronchioie were measured by evens blue dye and the total number and percentage of cells in the bronchoalveolar lavage fluid were calculated by HE dye. Results Stimulation by hot saline and 0.1 mol/L hydrochloric acid of the esophagus significantly increased the microvascular leakage of trachea and main bronchi （all P〈 0.05 ）, microvascular leakage of bronchiole also increased in hot saline group. Phosphoramidone could significantly potentiated plasma extravasation in the trachea, main bronchi and bronchiole （ P 〈0.05）.capsazepine inhibited the plasma extravasation of trachea and bronchial induced by hot saline and acid. The total number and percentage of cells in the bronchoalveolar lavage fluid in different groups showed no significant difference . Conclusions Hot saline and hydrochloric acid stimulation intraesophageal can induce microvasclur leakage of airway. TRPV1 and neuropeptide may play an important role in it.
出处
《国际呼吸杂志》
2009年第21期1281-1284,共4页
International Journal of Respiration
基金
本课题受国家自然科学基金（30871000）
广东省自然科学基金项目（8451018201001069）资助
关键词
热刺激
酸刺激
瞬时受体电位香草酸亚型1
神经肽
Heat stimulation
Acid stimulation
Transient receptor potential vanilloid 1
Neuropeptide
