Comparison of airway responses following tracheal or esophageal acidification in the cat.

Comparison of airway responses following tracheal or esophageal acidification in the cat.
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DOI:
10.5555/uri:pii:0016508584900829
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发表时间:
1984
期刊:
影响因子:
29.4
通讯作者:
D. Tuchman;J. Boyle;A. Pack;J. Scwartz;M. Kokonos;A. Spitzer;S. Cohen
D. Tuchman;J. Boyle;A. Pack;J. Scwartz;M. Kokonos;A. Spitzer;S. Cohen
中科院分区:
医学1区
文献类型:
--
作者:
D. Tuchman;J. Boyle;A. Pack;J. Scwartz;M. Kokonos;A. Spitzer;S. Cohen

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为了确定胃食管反流与阻塞性肺疾病之间关联的可能机制,我们定量比较了 13 只麻醉成年猫气管或食管输注酸后的短潜伏气道反应。总肺阻力是根据呼气末水平的气流和胸膜内压力差的同步测量来计算的。在所有测试的动物中,气管输注低至 0.05 ml 0.2 N HCl 时,总肺阻力相对于基线平均增加 4.65 倍(p 小于 0.005)。气管内注射生理盐水没有效果。对气管内输注酸的反应是快速适应的、pH 依赖性的和迷走神经介导的。将更大体积的 10 ml 0.2 N HCl 注入食道后,总肺阻力比基线平均增加 1.47 倍(p 小于 0.05)。食管内盐水未见变化。与气管内输注酸相反,在食管内酸化后测试的 13 只动物中,只有 8 只观察到阻力明显显着增加。当发生这种情况时,输注酸后反应持续至少 60 秒。严重食管炎的存在并没有增强反应的强度。这些研究强化了这样的概念:气管和食管的反射通路可以解释胃食管反流与阻塞性肺疾病之间的因果关系。结果支持这样的观点,即气管微抽吸是与胃食管反流相关的支气管痉挛比简单的胃酸反流到食管更有可能的机制。
To determine a possible mechanism for the association between gastroesophageal reflux and obstructive pulmonary disease, we quantitatively compared the short latent airway response after acid infusion into the trachea or esophagus in 13 anesthetized adult cats. Total lung resistance was calculated from synchronous measurements of air flow and intrapleural pressure differences from those at end expiratory level. Tracheal infusion of as little as 0.05 ml of 0.2 N HCl evoked an average 4.65-fold increase in total lung resistance from baseline in all animals tested (p less than 0.005). Intratracheal saline had no effect. The response to intratracheal acid infusion was rapidly adapting, pH dependent, and vagally mediated. Infusion of a much larger volume of 10 ml of 0.2 N HCl into the esophagus produced an average 1.47-fold increase in total lung resistance from baseline (p less than 0.05). No change was seen with intraesophageal saline. In contrast to intratracheal acid infusion, a clearly significant increase in resistance was seen in only 8 of 13 animals tested after intraesophageal acidification. When it occurred, the response was sustained for at least 60 s after acid infusion. The magnitude of the response was not augmented by the presence of severe esophagitis. These studies strengthen the concept that reflex pathways in the trachea and esophagus may explain a causal relationship between gastroesophageal reflux and obstructive pulmonary diseases. The results support the view that microaspiration into the trachea is a much more likely mechanism for bronchospasm associated with gastroesophageal reflux than simple acid reflux into the esophagus.