An Animal Model for Airway Sensory Deprivation Producing Obstructive Apnea with Postmortem Findings of Sudden Infant Death Syndrome

Abstract

A series of experiments was performed in rabbits to investigate the effects of airway sensory stimuli on upper airway patency. Pharyngeal airway closure was observed in rabbits breathing through a tracheostomy tube; pharyngeal patency was rapidly restored either by closing the tracheostomy tube, which forced the animals to resume nasal breathing, or by creating cyclical pressure changes in the nose and pharynx to stimulate respiratory tidal airflow. This airway opening effect of pressure fluctuations was eliminated by topical anesthesia of the airway mucosa, an observation suggesting that sensory stimulation from pressure change is needed for airway patency. The observation that dead animals have a patent pharyngeal airway that is resistant to collapse from negative intraluminal pressure, and animals breathing via a tracheostomy have a readily collapsible airway that is closed at zero transmural pressure, suggests that airway-constructing muscles close the airway when the animals breathe via the tracheostomy. Loss of electromyographic activity from airway-dilating muscles (genioglossus) was observed during tracheostomal breathing and was restored by cyclical pressure changes applied to the upper airway lumen; this observation further suppports the concept that airway reflexes responding to pressure regulate the activity of airway-dilating and airway-constricting muscles. Topical anesthesia of the upper airway mucous membrane, which eliminated these responses to pressure, was associated with an obstructed pharyngeal airway and death from apparent asphyxia in either pentobarbital-anesthetized adult animals or young animals without general anesthetic. Death resulting from airway obstruction in this manner was associated with postmortem findings of sudden infant death syndrome (pulmonary edema and pleural petechiae) in the majority of animals.