Tomita M, Matsuo K, Maehara N, Umezaki T, Shin T
Department of Otolaryngology, Saga Medical School, Japan.
Arch Otolaryngol Head Neck Surg. 1988 Mar;114(3):308-12. doi: 10.1001/archotol.1988.01860150090021.
To clarify the mechanisms of ischemic change in the vocal fold on phonation, model experiments were performed under various conditions by recording tissue oxygen pressure (Pto2) values under electrical stimulation of either the recurrent laryngeal nerves or external branches of the superior laryngeal nerves. In addition, autonomic nerve regulation of laryngeal vessels was estimated under administration of succinylcholine chloride. Oxygen pressures of the vocal fold were measured in the lamina propria and vocal muscle at the middle of the membranous portion. The Pto2 in the lamina propria showed a slight increase during lower-frequency stimulation and a slight decrease during higher-frequency stimulation of the recurrent laryngeal nerve. The Pto2 in the vocal muscle showed a decrease during stimulation of the recurrent laryngeal nerve. On the other hand, the Pto2 showed almost no change in the lamina propria or vocal muscle during stimulation of the external branch of the superior laryngeal nerve. It is supposed that an ischemic change in the vocal muscle on phonation results mainly from contraction of the vocal muscle. On the contrary, the ischemic change in the vocal mucosa on phonation does not appear to be directly caused by the contraction of the vocal muscle but by other factors, such as wavelike movement.
为阐明发声时声带缺血变化的机制，通过记录喉返神经或喉上神经外支电刺激下的组织氧分压（Pto2）值，在各种条件下进行了模型实验。此外，在给予氯化琥珀胆碱的情况下评估了喉血管的自主神经调节。在膜性部分中部的固有层和声带肌中测量声带的氧分压。喉返神经低频刺激时固有层的Pto2略有升高，高频刺激时略有下降。喉返神经刺激时声带肌的Pto2下降。另一方面，喉上神经外支刺激时固有层或声带肌的Pto2几乎没有变化。推测发声时声带肌的缺血变化主要是由声带肌收缩引起的。相反，发声时声带黏膜的缺血变化似乎不是直接由声带肌收缩引起的，而是由其他因素，如波浪状运动引起的。
