Laryngeal water receptors are insensitive to body temperature in neonatal piglets.

Heat stress and the laryngeal chemoreflex (LCR) have both been implicated as possible contributors to the sudden infant death syndrome (SIDS). We recently reported that moderate hyperthermia, induced in decerebrate piglets by external heating, substantially prolonged the LCR elicited by injecting 0.1 ml of water into the larynx through a prepositioned transnasal catheter. To examine the question of whether hyperthermia influences the responses of laryngeal water receptors, we recorded single fiber action potentials in fine strands of the superior laryngeal nerve (SLN) in decerebrate piglets while the larynx was filled with water or isotonic saline. Water receptors, identified by their much brisker response to water than to saline, were studied with body temperature at 37.9+/-0.2 degrees C, after warming the animal to 40.6+/-0.2 degrees C and after cooling back to 37.7+/-0.3 degrees C. The results show no effect of body temperature change, in this range, on the responses of the laryngeal water receptors and thus suggest that the potentiation of the LCR by hyperthermia is mediated by a central action.