Gestational nicotine exposure exaggerates hyperthermic enhancement of laryngeal chemoreflex in rat pups

Laryngeal chemoreflex (LCR) apnea occurs in infant mammals in response to water or other liquids in the laryngeal lumen and is suspected to contribute to some cases of the sudden infant death syndrome. We have previously found that the LCR is prolonged in neonatal piglets and rats that are warmed 1–3 °C above their normal body temperatures and that this prolongation is exaggerated in rat pups whose mothers have been exposed to cigarette smoke during pregnancy. We have therefore examined the effects on the LCR of combined prenatal nicotine exposure and brief postnatal hyperthermia. Nicotine was infused in pregnant rats via implanted osmotic minipumps (6.5 mg/kg per day) from gestational day 3 (G3) until G21, the day of delivery. Control animals received saline infusions. On postnatal days 4–12, LCR apnea and respiratory disruption, elicited by intralaryngeal water, were measured with and without hyperthermia in anesthetized pups. The results indicate that prenatal exposure to nicotine significantly exaggerates the hyperthermic prolongation of the LCR.