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食管酸对气道高反应性的可能影响机制。

Possible mechanisms of influence of esophageal acid on airway hyperresponsiveness.

作者信息

Stein Mark R

机构信息

Section of Allergy, Good Samaritan Medical Center, West Palm Beach, Florida, USA.

出版信息

Am J Med. 2003 Aug 18;115 Suppl 3A:55S-59S. doi: 10.1016/s0002-9343(03)00194-3.

DOI:10.1016/s0002-9343(03)00194-3
PMID:12928076
Abstract

Airway hyperresponsiveness is among the defining phenomena in asthma. In this article, 3 mechanisms are reviewed to explain how gastroesophageal reflux (GER) may influence airway hyperresponsiveness. First, microaspiration may cause not only direct tissue injury, but may also trigger vagal reflexes. Second, acid infusion of the esophagus in a dog model and in humans has been shown to result in vagally mediated reflexes leading to bronchoconstriction. These reflexes have been studied using immunohistochemical techniques. Third, neuroinflammatory reflexes have been found to play a role in airway responses through the release of tachykinins, including substance P and neurokinin A. Combined, these 3 mechanisms may lead to an increase in vagal efferent impulses that can cause or augment airway hyperresponsiveness. Studies indicate that there is an increase in airway responsiveness in asthma patients who have documented GER. Further, based on the reported number of reflux episodes occurring during 24-hour pH monitoring, airway hyperresponsiveness to methacholine challenge tends to increase as GER worsens.

摘要

气道高反应性是哮喘的典型现象之一。在本文中,我们回顾了三种机制,以解释胃食管反流(GER)如何影响气道高反应性。首先,微量误吸不仅可能导致直接的组织损伤,还可能触发迷走神经反射。其次,在犬模型和人类中,向食管注入酸已被证明会导致迷走神经介导的反射,从而引起支气管收缩。这些反射已通过免疫组织化学技术进行了研究。第三,已发现神经炎症反射通过释放速激肽(包括P物质和神经激肽A)在气道反应中起作用。综合起来,这三种机制可能导致迷走神经传出冲动增加,从而引起或加剧气道高反应性。研究表明,有GER记录的哮喘患者气道反应性增加。此外,根据24小时pH监测期间报告的反流发作次数,随着GER恶化,对乙酰甲胆碱激发试验的气道高反应性往往会增加。

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Possible mechanisms of influence of esophageal acid on airway hyperresponsiveness.食管酸对气道高反应性的可能影响机制。
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