Inspiratory Activation of the Vocal Cord Adductor, Part II: Animal Study in the Cat.

Autor: Yasuko Sekita, Keisuke Shiba, Ken Nakazawa, Tamaki Numasawa, Shiroh Isono
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Zdroj: Laryngoscope; Feb2004, Vol. 114 Issue 2, p376-380, 5p
Abstrakt: SUMMARY: OBJECTIVES/HYPOTHESIS The authors have shown previously that the vocal cord adductor is activated during inspiration in patients with vocal cord abduction impairment and that this adductor inspiratory activity is abolished by relief from inspiratory tracheal negative pressure by opening the tracheostoma. (Shiba K. Isono S, Sekita Y, Tanaka A. Inspiratory activation of the vocal cord adductor, Part I: human study in patients with restricted abduction of the vocal cords. Laryngoscope 2004;114:372-375). The authors hypothesized that insufficient opening of the glottis during inspiration generates strong negative pressure in the trachea and that this negative pressure triggers an airway reflex that activates the adductor.STUDY DESIGN Experimental study of the mechanism of laryngeal obstruction using an animal model of restricted abduction of the vocal cords.METHODS To identify such an airway reflex, the authors recorded the adductor electromyogram in anesthetized cats whose vocal cords were mechanically adducted by stitching both cords together. To determine whether this reflex modulation of adductor activity is induced through afferents from the larynx or from the lower airway, the authors applied negative pressure to the subglottic space and lower airway separately.RESULTS The adductor was activated during inspiration with powerful negative pressure in the trachea. Negative pressure in the subglottic space had a more marked effect on the adductor activity than did pressure in the lower airway. The adductor inspiratory activity was virtually abolished by laryngeal deafferentation.CONCLUSION Glottal narrowing during inspiration reflexly activates the vocal cord adductor. This paradoxical inspiratory-related adductor activation is induced by an airway reflex triggered mainly through afferents from the larynx and probably contributes to stridor and dyspnea in patients with laryngeal obstruction. [ABSTRACT FROM AUTHOR]
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