Changes in Laryngeal Muscle Activities During Hypercapnia in the Cat

LETTERS TO THE EDITOR Changes in Laryngeal Muscle Activities During Hypercapnia in the Cat To the Editor: In their recent article (1998;118:537-44), Adachi et al studied changes in laryngeal muscle activities during hypercapnia in the decerebrate cat. They reported that an increase in phasic expiratory thyroarytenoid muscle activity under hypercapnic conditions results in glottic constriction during expiration. A systematic analysis of the EMG activity was not performed. Instead, the authors used endotracheal pressure to determine the effect of laryngeal muscle activity on glottic size. However, endotracheal pressure was measured with the animals breathing through the nose and mouth. This experimental design does not permit an assessment of laryngeal function given that activation of respiratory pump muscles during expiration under hypercapnic conditions will increase endotracheal pressure independent of glottic size. Results similar to those reported by Adachi et al can be obtained under hypercapnic conditions measuring endotracheal pressure in a tracheotomized decerebrate cat (ie, with the larynx eliminated from the breathing circuit). To accurately assess the mechanical effects of hypercapnia on laryngeal function, the authors should have used an isolated upper airway preparation, with the animal breathing through a caudal tracheotomy cannula and a constant flow of air being passed in a retrograde direction through a rostral tracheal cannula. l The authors' conclusions are invalid because of the lack of quantitative EMG data and the faulty experimental design of their study. Samuel T. Kuna, MD Associate Professor Department of Internal Medicine University of Texas Medical Branch at Galveston 5.112 John Sealy Annex 301 University Blvd Galveston, TX 77555-0561 23/8/94997

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ment of the vocal cords, whereas the adductor muscles were silent during eucapnia. In these studies the posterior cricoarytenoid muscle not only increased its activities but also prolonged its duration to expiration beyond the inspiratory phase during hypercapnia. On the contrary, some previous studies reported that the abductor muscle was active in inspiration and the adductor muscles were active in expiration during eucapnia and, furthermore, that both the abductor and adductor muscles increased their activities during hypercapnia compared with those during eucapnia, as mentioned in our article. A recent study using a decerebrated and paralyzed cat also demonstrated that the recurrent laryngeal nerve activity during expiration was recruited by hypercapnia of 8% end-tidal CO 2 ,] We also observed changes of the activities of laryngeal motoneurons, which were located in the nucleus ambiguus of the medulla oblongata, caused by hypercapnia. Some part of both inspiratory and expiratory laryngeal motoneurons increased or recruited their activities during hypercapnia. 2 In this study we emphasized that the laryngeal adductor muscles increased their activities during hypercapnia compared with those during eucapnia and that this increase of the adductor muscle activities inevitably induces an increase of the laryngeal resistance on expiration. We do not think that measurement of the laryngeal resistance under unphysiologic condition is necessary. The increase of endotracheal pressure on expiration during hypercapnia was caused by various physiologic phenomena, such as respiratory facilitation and the shapes of the oral and nasal cavities. We do not think that the increase of endotracheal pressure on expiration during hypercapnia is ever caused by only the increase of the adductor muscle activity. We regard the endotracheal pressure as the total effect induced by various physiologic changes during hypercapnia. Finally, it was confirmed in our study using spontaneously breathing cats more natural than those with the airway separated that the endotracheal pressure is maintained at a higher level through the expiratory phase during hypercapnia than during eucapnia. We believe that Dr Kuna's comments concerning our article result from a misinterpretation, and we are anxious that our article should be estimated appropriately.

1. Barlett D Jr. Effects of hypercapnia and hypoxia on laryngeal resistance to airflow. Respir Physiol 1979:37:293-302.

Authors 'Reply: Dr Kuna estimates our investigation about changes in laryngeal muscle activities during hypercapnia to be invalid because of the lack of quantitative EMG data. In our Figs I and 2, however, it was clearly demonstrated that during hypercapnia both the laryngeal abductor muscle and the adductor muscle increased their activities during the inspiratory and expiratory phases, respectively, compared with those during eucapnia; thus we did not think that quantitative analysis of the EMG activities was necessary. Until recently, many studies reported that only the posterior cricoarytenoid muscle participated in respiratory moveMarch 1999

Tomoyuki Adachi, MD Toshiro Umezaki, MD Department of OtolaryngologyHead and Neck Surgery Saga Medical School 5-5-1 Nabeshima Saga, Japan 849-8501 23/8/94998

REFERENCE 1. Shiba K, Umezaki T. Zheng Y, et al. Ficative vocalization in the cat. Neuroreport 1996:7:2139-42. 2. Umezaki T, Matsuse T. Adachi T, et al. Changes in excitability of laryngeal motoneurons on respiratory rhythm in the cat. Jpn J Physiol Supp! 1994;44(Suppl I).

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