Sina Nasri Ali Namazie Ming Ye Joel A. Sercarz Jody Kreiman Bruce R. Gerratt Gerald S. Berke
Div. of Head and Neck Surgery, UCLA School of Medicine, 10833 Le Conte Ave., Los Angeles, CA 90024-1624
Previous studies of laryngeal biomechanics using in vivo models have generally used a constant air flow source. Several authors have recently suggested that during phonation, the lung--thorax system functions as a constant pressure source. The present paper describes an in vivo canine system designed to maintain a constant peak subglottic pressure (P[sub sub]) using a pressure-controlling mechanism. It was found that with a decrease in P[sub sub], the range of recurrent laryngeal nerve stimulation (RLNS) voltage needed to induce phonation was reduced. At a given superior laryngeal nerve stimulation (SLNS) level and P[sub sub], increasing levels of RLNS resulted in a normal distribution of vocal efficiencies. For each SLNS and P[sub sub], minimum and maximum levels of RLNS were determined outside of which no phonation was possible. Levels of RLNS that produced an optimal stable phonation were also identified. Increasing levels of RLNS resulted in significant decreases in glottal air flow. Contrary to a previous report using a constant flow source, increasing levels of SLNS produced a significant decrease in glottal resistance. This is consistent with another previous study [D. M. Moore and G. S. Berke, J. Acoust. Soc. Am. 83, 705--714 (1988)] demonstrating that the open quotient increased with increasing SLNS.