Laryngeal reflex apnea in neonates: Effects of CO2 and the complex influence of hypoxia

We have examined influence of hypocapnia, mild hypercapnia and hypoxia on the durations of fictive apnea and respiratory disruption elicited by injection of 0.1 ml of water into the laryngeal lumen-the laryngeal chemoreflex (LCR)-in 20 unanesthetized, decerebrate, vagotomized piglets aged 4-10 days that were paralyzed and ventilated with a constant frequency and tidal volume. The LCR was enhanced by hypocapnia and attenuated by hypercapnia as reported by others. The responses to laryngeal stimulation during hypoxia were varied and complex: some animals showed abbreviated responses during the tachypnea of early hypoxia, followed after 10-15 min by more prolonged apnea and respiratory disruption accompanying the reduction in ventilatory activity that commonly occurs during sustained hypoxia in neonates. We speculate that this later hypoxic enhancement of the LCR may be due to accumulation of adenosine in the brain stem.

► We measured the laryngeal chemoreflex (LCR) in decerebrate neonatal piglets. ► LCR-induced apnea (LCR-A) was prolonged by hypocapnia and shortened by hypercapnia. ► In hypoxia some piglets had biphasic responses of respiratory frequency and LCR-A. ► Prolonged LCR-A in hypoxia may be a trigger for the Sudden Infant Death Syndrome.