Mechanisms of active laryngeal closure during noninvasive intermittent positive pressure ventilation in nonsedated lambs.

The present study stems from our recent demonstration (Moreau-Bussiere F, Samson N, St-Hilaire M, Reix P, Lafond JR, Nsegbe E, Praud JP. J Appl Physiol 102: 2149-2157, 2007) that a progressive increase in nasal intermittent positive pressure ventilation (nIPPV) leads to active glottal closure in nonsedated, newborn lambs. The aim of the study was to determine whether the mechanisms involved in this glottal narrowing during nIPPV originate from upper airway receptors and/or from bronchopulmonary receptors. Two groups of newborn lambs were chronically instrumented for polysomnographic recording: the first group of five lambs underwent a two-step bilateral thoracic vagotomy using video-assisted thoracoscopic surgery (bilateral vagotomy group), while the second group, composed of six lambs, underwent chronic laryngotracheal separation (isolated upper airway group). A few days later, polysomnographic recordings were performed to assess glottal muscle electromyography during step increases in nIPPV (volume control mode). Results show that active glottal narrowing does not develop when nIPPV is applied on the upper airways only, and that this narrowing is prevented by bilateral vagotomy when nIPPV is applied on intact airways. In conclusion, active glottal narrowing in response to increasing nIPPV originates from bronchopulmonary receptors.

Origins of the inhibiting effects of nasal CPAP on nonnutritive swallowing in newborn lambs.

The present study investigated the mechanism by which continuous positive airway pressure (CPAP) suppresses nonnutritive swallowing (NNS) during quiet sleep (QS) in newborn lambs. Eighteen full-term lambs were chronically instrumented and evenly distributed into three separate groups to determine the extent to which modulation of NNS may be attributed to stimulation of upper airway and/or bronchopulmonary mechanoreceptors. Six lambs were tracheotomized, six other lambs underwent a two-step bilateral intrathoracic vagotomy, and the remaining six lambs underwent chronic laryngotracheal separation (isolated upper airway group). Forty-eight hours after surgery, each nonsedated lamb underwent polysomnographic recordings on three consecutive days. States of alertness, NNS and respiratory movements were recorded. Results demonstrate that a CPAP of 6 cmH(2)O inhibited NNS during QS while administered directly on the lower airways and that bivagotomy prevented this inhibition. However, application of CPAP on the upper airways only also inhibited NNS during QS. Finally, the application of a CPAP of 6 cmH(2)O had no systematic effect on NNS-breathing coordination (assessed by the respiratory phase preceding and following NNS). In conclusion, our results suggest that bronchopulmonary receptors are implicated in the inhibiting effects of nasal CPAP of 6 cmH(2)O on NNS in all our experimental conditions, whereas upper airway receptors are only implicated in certain conditions.