A pressure-regulated model of normal and pathologic phonation.

Recent evidence suggests that the lung-thorax system functions as a constant pressure source during phonation. However, previous animal models used a constant flow source. This article describes an in vivo canine model that maintains a constant subglottic pressure during phonation to more closely simulate the pulmonary system. At any given subglottic pressure, increasing levels of recurrent laryngeal nerve stimulation resulted in a significant rise in resistance followed by a plateau. Increasing levels of superior laryngeal nerve stimulation, however, produced no significant change in glottal resistance. Three experimental conditions were studied: normal, unilateral recurrent laryngeal nerve paralysis, and paralysis followed by arytenoid adduction. In normal canines, maximal vocal efficiency values were the highest, indicating the best match between pressure and resistance. The vocal efficiency values were significantly lower in recurrent laryngeal nerve paralysis, indicating pressure-resistance mis-match. Arytenoid adduction increased the maximal vocal efficiency values and decreased the mismatch observed in the paralyzed state. These findings may provide insight into an understanding of normal and pathologic laryngeal behavior.