Effects of postnatal smoke exposure on laryngeal chemoreflexes in newborn lambs
Laryngeal chemoreflexes (LCR), which are elicited by the contact of liquids such as gastric refluxate with laryngeal mucosa, may trigger some cases of sudden infant death syndrome. Indeed, while LCR in mature mammals consist in lower airway protective responses, previous animal data have shown that LCR in immature newborns can include laryngospasm, apnea, bradycardia and desaturation. The present study was aimed at testing the hypothesis that postnatal exposure to cigarette smoke is responsible for enhancing cardiorespiratory inhibition observed with LCR. Eight lambs were exposed to cigarette smoke (20 cig/day) during 16 days and compared to seven control lambs. Urinary cotinine/creatinine ratio was measured at a level relevant to previously published levels in infants. On D15-D16, 0.5 ml of HCl (pH 2), milk, distilled water or saline was injected onto the larynx via a chronic supra-glottal catheter during sleep. Results showed that exposure to cigarette smoke significantly enhanced apneas and bradycardias during LCR while significantly decreasing swallowing and arousal. These results were observed independently of the state of alertness and of the experimental solution tested. In conclusion, 15 day-postnatal exposure to cigarette smoke increases cardiorespiratory inhibition and decreases lower airway protective mechanisms in non-sedated, full-term lambs.