Prolonged active glottic closure after barbiturate-induced respiratory arrest in lambs.

We recently showed that the glottis is actively closed throughout post-hyperventilation, hypocapnic central apnea in lambs. The present study was designed to test whether the glottis is also closed in non-hypocapnic central apnea. Twenty-seven lambs aged 2 to 30 days were intravenously injected with 325 mg of sodium pentobarbital, so as to obtain breathing arrest. Airflow was recorded via a facial mask and pneumotachograph, along with the electromyographic activity (EMG) of the thyroarytenoid muscle (TA, a glottic adductor). With the onset of apnea, continuous TA EMG appeared in a few seconds and rose rapidly. Brief inspiratory gasps were observed in eight lambs, and TA EMG was abruptly inhibited for the exact duration of the gasps. The continuous TA EMG then disappeared after 115 to 230 sec. We conclude that the glottis is actively closed during fatal non-hypocapnic central apnea in lambs. Our data suggest that active glottic closure occurs with major depression of central inspiratory drive.

Laryngeal response to hypoxia in awake lambs during the first postnatal days.

We recently showed that hypoxia does not induce active expiratory glottic adduction in awake lambs more than 10 d old. To reconcile our results with previous data from other researchers, we hypothesized that an active expiratory glottic closure might still be part of the response to hypoxia in the very first postnatal days. The present study was undertaken to test this hypothesis. We studied 22 awake, nonsedated lambs during hypocapnic hypoxia (fraction of inspired O2 = 0.08 during 15 min) induced during the first 72 h of postnatal life. We recorded airflow via a facial mask and pneumotachograph, along with the electromyographic activity (EMG) of the thyroarytenoid muscle (a glottic adductor) in 10 lambs. We also recorded the EMG of both the posterior cricoarytenoid (n = 4) and cricothyroid (n = 5) muscles (glottic abductors), as well as the abdominal muscles (n = 4). We identified typical expiratory airflow braking on the breath-by-breath computed flow-volume loop and thyroarytenoid muscle expiratory EMG as evidence of active expiratory glottic adduction. We found that hypoxia induced a biphasic ventilatory response, with an early peak and a subsequent decrease, and that active expiratory glottic adduction was absent during baseline room-air breathing and hypoxia. We also found that the glottic abductor phasic inspiratory and tonic expiratory EMG as well as the abdominal muscle phasic expiratory EMG, all of which were present during baseline recording, increased during hypoxia. We conclude that hypoxia does not induce expiratory glottic closure in the very first days of life in awake lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Thyroarytenoid muscle activity during hypocapnic central apneas in awake nonsedated lambs.

In this study, we examined whether the glottis is open or closed during central apnea and the effect of arterial PO2 (PaO2) on this control. We hyperventilated nine 11- to 30-day-old awake nonsedated lambs via a tracheostomy for 1 min to induce central apnea. Four gas mixtures (8, 15, 21, and 30% O2) were used. At the end of the hyperventilation period, the lambs were allowed to breathe spontaneously through intact 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 adductor), the posterior cricoarytenoid muscle (PCA, laryngeal abductor), the cricothyroid muscle (CT), and the diaphragm. We found that hyperventilation consistently induced hypocapnic central apnea in all nine lambs in hyperoxic conditions [30% inspiratory fraction of O2 (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 activity or expiratory airflow braking. Continuous TA EMG activity began early during hyperventilation and continued throughout the central apnea, regardless of PaO2. The first 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.(ABSTRACT TRUNCATED AT 250 WORDS)