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Acid-induced laryngospasm in a canine model

C J Loughlin¹, J A Koufman, D B Averill

¹Center For Voice Disorders, Department of Otolaryngology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, NC 27157-1034, USA.

The Laryngoscope

|December 1, 1996

Summary

Canine laryngeal responses to acid stimulation were studied. Acid at pH 2.5 or less triggered laryngospasm, mediated by superior laryngeal nerves, not recurrent laryngeal nerves.

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Area of Science:

Otolaryngology
Neuroscience
Gastroenterology

Background:

Gastroesophageal reflux disease (GERD) can cause laryngeal symptoms.
The specific laryngeal mechanisms triggered by acid reflux are not fully understood.

Purpose of the Study:

To investigate the efferent laryngeal responses to topical acid and pepsin stimulation in a canine model.
To identify the neural pathways involved in acid-induced laryngospasm.

Main Methods:

Electromyographic recordings of the thyroarytenoid muscle in dogs.
Sequential instillation of hydrochloric acid at varying pH levels and pepsin into the larynx.
Bilateral sectioning of the superior laryngeal nerves followed by repeat stimulation.

Main Results:

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Laryngospasm occurred in all dogs when laryngeal pH reached 2.5 or less.
Control substances (saline, water, pepsin alone) did not induce laryngospasm.
Acid-induced laryngospasm was abolished after superior laryngeal nerve sectioning, while capsaicin still induced it.

Conclusions:

pH-sensitive chemoreceptors in the canine larynx trigger laryngospasm at pH 2.5 or lower.
These acid-sensitive receptors are innervated by the superior laryngeal nerves.
Subglottic chemoreceptors responsive to capsaicin are supplied by the recurrent laryngeal nerves.