Prenatal nicotine exposure exaggerates thermal prolongation of the laryngeal chemoreflex in rat pups

Abstract

Laryngeal chemoreflex (LCR) apnea occurs in infants in response to water in the larynx and may contribute to pathogenesis of SIDS. The LCR is prolonged in neonatal piglets and rats that are warmed 1‐3 degrees C, and this thermal prolongation is exaggerated in rat pups born to mothers exposed to cigarette smoke during pregnancy. Since smoking mothers expose their fetuses to nicotine, we studied the effect on the LCR of combined prenatal nicotine exposure and brief postnatal hyperthermia in anesthetized rat pups. Pregnant rats were exposed to nicotine (6.4 mg/kg/day) or saline by infusion via implanted osmotic minipumps from gestational day 3 (GD3) until GD 21. The LCR was assessed between postnatal days 4‐15 with and without hyperthermia. Prenatal nicotine exposure exaggerated the thermal prolongation of the LCR. In the nicotine group (n=21), respiratory disruption by the LCR during hyperthermia averaged 13.24 1.85 sec, and the longest apnea averaged 8.29 1.29 sec. In the control group (n=24), respiratory disruption under the same conditions averaged 7.19 0.97 sec, and the longest apnea averaged 4.68 0.76 sec. Thus, prenatal nicotine exposure enhances the hyperthermic prolongation of the LCR, which has previously been shown in piglets to depend on GABAergic inhibition of breathing.(Supported by P01‐HD36379, HD042707 and a grant from the Flight Attendants Medical Research Institute.)