Cardiac effects of esophageal stimulation: possible relationship between gastroesophageal reflux (GER) and sudden infant death syndrome (SIDS).
Twenty-six artificially ventilated newborn pigs were subjected to simulated gastroesophageal reflux; saline (10 cc) of varying pH was flushed through the esophagus from below. At a given pH threshold, reflex bradycardia, which could be blocked by atropine, was elicited. Transecting of the superior laryngeal nerves, the recurrent laryngeal nerves, and the pharyngeal plexus nerves did not block the reflex bradycardia. However, bypassing the regions superior to the esophagus with a shunt prevented the bradycardia. These results indicate that bradycardia caused by gastroesophageal reflux is independent of changes in ventilation and may be an important cause of sudden infant death.
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001919:Bradycardia / Q000150:complications / Q000209:etiology*; D004195:Disease Models, Animal; D005764:Gastroesophageal Reflux / Q000150:complications*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007223:Infant; D007823:Laryngeal Nerves / Q000601:surgery; D010614:Pharynx / Q000294:innervation; D012009:Recurrent Laryngeal Nerve / Q000601:surgery; D012965:Sodium Chloride / Q000494:pharmacology; D013398:Sudden Infant Death / Q000209:etiology*; D013552:Swine
D012965:Sodium Chloride