Attenuated oxygen sensifitivy after prenatal nicotine exposure-evidence for a dopaminergic mechanism. † 1797

Abstract

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.