I. Kianicka et al., THYROARYTENOID MUSCLE-ACTIVITY DURING HYPOCAPNIC CENTRAL APNEAS IN AWAKE NONSEDATED LAMBS, Journal of applied physiology, 76(3), 1994, pp. 1262-1268
In this study, we examined whether the glottis is open or closed durin
g central apnea and the effect of arterial P-o2 (Pa-o2) on this contro
l. We hyperventilated nine 11- to 30-day-old awake nonsedated lambs vi
a a tracheostomy for 1 min to induce central apnea. Four gas mixtures
(8, 15, 21, and 30% O-2) were used. At the end of the hyperventilation
period, the lambs were allowed to breathe spontaneously through intac
t upper airways. Using a pneumotachograph attached to a face mask, we
measured airflow, and we continuously recorded electromyographic (EMG)
activity of the thyroarytenoid (TA), the main glottic adductor muscle
. We also studied the lateral cricoarytenoid muscle (LCA, laryngeal ad
ductor), the posterior cricoarytenoid muscle (PCA, laryngeal abductor)
, the cricothyroid muscle (CT), and the diaphragm. We found that hyper
ventilation consistently induced hypocapnic central apnea in all nine
lambs in hyperoxic conditions [30% inspiratory fraction of O-2 (FIo2)]
in eight of nine lambs in normoxia or mild hypoxia (15 and 21% FIo2),
and in four of seven lambs in hypoxia (8% FIo2). During baseline room
air breathing, there was no glottic adductor muscle expiratory EMG ac
tivity or expiratory airflow braking. Continuous Th EMG activity began
early during hyperventilation and continued throughout the central ap
nea, regardless of Pa(o2)irst subsequent breathing efforts were marked
by expiratory flow braking and expiratory activity of the TA. The LCA
and the TA demonstrated the same EMG activity pattern. Conversely, th
e activity of the glottic abductor (PCA), the CT, and the diaphragm (p
hasically active in inspiration during baseline room air breathing) di
sappeared during the hyperventilation period, was nil throughout centr
al apnea, and resumed with the first inspiratory efforts. Thus, in awa
ke nonsedated lambs, hypocapnic central apneas were accompanied by con
tinuous glottic adduction regardless of Pa-o2. This combination could
prevent alveolar gas from flowing out of the lung, thus permitting con
tinuous alveolar blood gas exchanges during central apnea.