Maternal smoking is associated with the sudden infant death syndrome. Exposure to nicotine or tobacco smoke impairs hypoxic defense mechanisms in young animals and human infants. Nicotine enhances the release of the neuromodulator dopamine (DA) in the brain. Increased DA content in the carotid bodies (CB), and in the brain stem (BS) attenuates the ventilatory responses to changes in FiO2. The study hypothesis was that antenatal nicotine exposure during the last trimester decreases ventilatory responses to changes in FiO2 through a dopaminergic mechanism in CB or BS. Subjects& Methods: Hyperoxic tests (change in minute ventilation (Vdot1) to FiO2 1.0 for 10 sec or 5 breaths) were performed in 3 groups of awake, 3-14 d old lambs: 8 controls (CTRL), 6 prenatally nicotine treated (PT) and 6 pre- and postnatally treated (PPT) by implanted minipumps. Hyperoxic tests were performed during infusion of a) saline, b) domperidone (domp), a DA2 receptor blocker in CB or c) SCH 23390, a DA1 receptor blocker in the BS.
Results: Nicotine treated lambs had a lower response to hyperoxia than controls. Either SCH or domp restored the response in nicotine treated but had no effect in control lambs.
Hyperoxic tests (% change in Vdot1) Table
Conclusion: Prenatal nicotine exposure reduces the ventilatory response to hyperoxia through dopaminergic modulation of oxygen sensitivity at both a central and a peripheral level.
Speculation: Prenatal nicotine may impair hypoxic defense in young mammals through a dopaminergic mechanism. (HD 28916 and HL 14214).
About this article
Cite this article
Hafström, O., Milerad, J., Poole, S. et al. Attenuated oxygen sensifitivy after prenatal nicotine exposure-evidence for a dopaminergic mechanism. † 1797. Pediatr Res 41, 302 (1997). https://doi.org/10.1203/00006450-199704001-01816
Respiratory Physiology & Neurobiology (2005)