Maternal omega‐3 supplementation reduces apnea duration induced by laryngeal chemoreflex stimulation in rat pups

The laryngeal chemoreflex (LCR) is a series of responses activated when fluids or solids come into contact with the laryngeal mucosa to prevent their aspiration into the airways. In preterm infants LCR triggers apneas, bradycardias, and O 2 desaturations that can be life threatening. Because fatty acids omega‐3 (Ω‐3) benefit brain development, we tested the hypothesis that Ω‐3 reduces the deleterious cardio‐respiratory consequences resulting from LCR stimulation in rat pups. Experiments were performed on pups (10‐11 days old). Pups were raised by mothers that were either fed a normal diet (control; 3g/kg of Ω‐3) or received an Ω‐3 enriched diet (13g/kg of Ω‐3) from birth to day 10‐11. Pups were anesthetized (chloralose 20mg/kg + urethane 1mg/kg). A tracheotomy was performed below the larynx to place a water filled catheter near the larynx. Breathing was monitored with an EMG electrode on the intercostals muscle. O 2 saturation and heart rate were monitored with pulse oxymetry. Following baseline measurements of cardio‐respiratory variables, each pup received 10 µL injection of water near the larynx. This procedure was repeated 3 times with a 5 min recovery period between injections. By comparison with controls, maternal Ω‐3 supplementation effectively raised Ω‐3 levels in the blood and brainstem of the pups and reduced apnea duration elicited by LCR stimulation by 32%. These data suggest that Ω‐3 supplementation accelerates development of the brainstem circuits that regulate breathing. Subsequent work will evaluate the effect on respiratory variables in intact pups. These results suggest that maternal Ω‐3 supplementation may alleviate cardio‐respiratory complications associated with neurological immaturity.