Laryngeal narrowing during nasal ventilation does not originate from bronchopulmonary C-fibers

Abstract

We previously showed that nasal pressure support ventilation (nPSV) can lead to active inspiratory laryngeal narrowing, which originates from the stimulation of bronchopulmonary receptors. Among the three major types of bronchopulmonary receptors, which are variably stimulated by lung distension, C-fiber endings are remarkable, given that their stimulation can also trigger laryngeal closure. Taking advantage of our lamb model with blocked C-fibers, we aimed to assess whether bronchopulmonary C-fiber endings are involved in the active inspiratory laryngeal narrowing during nPSV. Nine lambs were surgically instrumented to assess states of alertness, electrical activity of a glottal constrictor (EaTA), respiratory movements and arterial blood gases. Forty-eight hours later, two polysomnographic recordings were performed during nPSV 15/4 cmH 2 O, before and after C-fiber blockade. During nPSV, blockade of C-fibers did not prevent inspiratory EaTA (present for 74 ± 41% of respiratory cycles vs. 64 ± 35%, p = 0.9). We conclude that active inspiratory laryngeal narrowing during nPSV does not originate from bronchopulmonary C-fiber endings.

The contribution of ovine models to perinatal respiratory physiology

“…On the contrary, nasal neurally-adjusted ventilatory assist (178) and nasal high-frequency oscillatory ventilation (179) do not induce active inspiratory laryngeal narrowing. The reflex inspiratory closure of the larynx in nasal pressure support ventilation has been shown to originate from bronchopulmonary mechanoreceptors (180,181), and to be prevented by permitting moderate hypercapnia (182).…”