Hypoxia and Hypercapnia Attenuate the Increase in Laryngeal Motor Nerve Activity Produced by Electrical Stimulation of the Superior Laryngeal Nerves.♦ 1636

Abstract

In the unanesthetized, decerebrate piglet, electrical simulation of the superior laryngeal nerve (SLN Stim) during mid inspiration results in phrenic apnea that persists beyond the end of the stimulus. We have previously shown that the phrenic apnea produced by SLN Stim is attenuated during hypoxia. To evaluate the effects of SLN Stim on laryngeal motor nerve activity, we studied 23 piglets (1-4 weeks of age; unanesthetized, decerebrate, vagotomized in the chest, paralyzed, ventilated) to determine the effects of SLN Stim on the activity of the phrenic nerve (PHR), and the thyroarytenoid (TA) and posterior cricoarytenoid (PCA) branches of the recurrent laryngeal nerve during sequential, randomly ordered exposure to 100% and 10% O2, 9% CO2, and 1% CO, and after injecting NaCN into one carotid bifurcation (CB). Under all conditions, whereas PHR and PCA activity ceased in response to SLN Stim, TA activity increased dramatically (>200% of normal peak activity, P < 0.001). After a 3 sec SLN Stim during baseline hyperoxic conditions, TA activity remained tonically elevated for an additional 14.4 ± 3.6 seconds. The post-SLN Stim tonic elevation of TA activity was attenuated to 2.1 ± 0.3 sec, 2.9 ± 0.7 sec, 2.0 ± 0.4 sec, and 1.9± 0.2 sec during ventilation with 10% O2, 9% CO2, 1% CO, and after CB NaCN injection, respectively (P<0.05). In 4 additional animals, surgical denervation of the carotid bodies together with a mid cervical vagotomy appeared to decrease the attenuating effects of hypoxia on phrenic apnea produced by SLN Stim. In addition, on average, baseline TA activity remained elevated for several breaths after resumption of PHR, TA, and PCA cycling. These results support the hypothesis that SLN stim increases post-inspiratory neural activity, while largely inhibiting inspiratory activity. These alterations are attenuated by hypoxia and hypercapnia. The effects of hypoxia appear to be dependent on stimulation of peripheral chemoreceptors. Under natural conditions, the loss of diaphragm and laryngeal dilator activity with an increase in laryngeal constrictor activity might increase the probability of airway obstruction, particularly during recovery after laryngeal stimulation. We speculate that hypoxia and hypercapnia provide a“protective” function, attenuating the both the respiratory inhibitory and upper airway obstructive effects of laryngeal stimulation.