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Laryngoscope. 1996 Dec;106(12 Pt 1):1506-9.

Acid-induced laryngospasm in a canine model.

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


A canine model was used to investigate the efferent laryngeal responses to stimulation by topically applied acid and pepsin. Five adult mongrel dogs were studied. Electromyographic recordings from the thyroarytenoid muscle were measured with hooked-wire electrodes as an acid solution (normal saline/hydrochloric acid at pH 6.0, 5.0, 4.0, 3.0, 2.5, 2.0, 1.5, and 1.0) was sequentially instilled into the larynx. Laryngospasm (tonic, sustained contraction of the thyroarytenoid muscle) occurred in all animals at pH 2.5 to 2.0 or less. Control substances such as neutral pH isotonic saline, hypotonic saline, hypertonic saline, water, and pepsin alone failed to produce laryngospasm. Next, solutions containing both acid (in the same pH range) and pepsin were tested. The laryngeal responses were similar to those of acid alone. The superior laryngeal nerves were sectioned bilaterally and the above experiments repeated. None of the test solutions produced laryngospasm; however, when capsaicin (1%) was instilled into the subglottis, laryngospasm occurred. Thus, chemoreceptors in the subglottis (supplied by the recurrent laryngeal nerves) appear to be responsive to capsaicin stimulation but not to acid stimulation. The data suggest that pH-sensitive chemoreceptors in the canine larynx cause laryngospasm (when the pH of the test solution is 2.5 or less) and that these acid receptors are supplied by the superior laryngeal nerves.

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