Systemic administration of Interleukin‐1beta enhances thermal prolongation of the laryngeal chemoreflex in decerebrate piglets—implications for Sudden Infant Death Syndrome

Abstract

The laryngeal chemoreflex (LCR) causes apnea and may initiate the process leading to the Sudden Infant Death Syndrome (SIDS). Recent upper respiratory tract infection (URI) and thermal stress are risk factors for SIDS, and elevating body temperature in decerebrate piglets prolongs the duration of LCR apnea. We tested the hypothesis that administering interleukin‐1beta (IL‐1b), a cytokine that is elevated by URIs and in turn elevates body temperature, would enhance thermal prolongation of the LCR. Decerebrate piglets (P4 to P13) were tracheostomized, paralyzed and ventilated, and 0.1 ml of water was introduced into the larynx to elicit the LCR. We recorded the duration of phrenic apnea and respiratory disruption associated with the LCR at normal body temperature and when body temperature was elevated by 2 degrees C. Pretreatment by intraperitoneal (IP) administration of IL‐1b (3 microgm/Kg) enhanced thermal prolongation of the LCR compared to control animals treated simultaneously with 10 mg/Kg IP indomethacin and IL‐1b. We conclude that IL‐1b enhances thermal prolongation of the LCR through a mechanism that requires synthesis of additional inflammatory mediators.Support: grants 36379 & 42707 from the NICHD