Respiratory Physiology & Neurobiology 143 (2004) 1–8 Influence of prenatal nicotine exposure on postnatal development of breathing pattern Yu-Hsien Huang, Amanda R. Brown, Seres Costy-Bennett, Zili Luo, Ralph F. Fregosi ∗ Department of Physiology, The University of Arizona, Tucson, AZ 85721-0093, USA Accepted 19 July 2004 Abstract To determine if prenatal nicotine exposure alters the postnatal development of the ventilatory pattern and the frequency and duration of apneas, we recorded respiratory airflow with head-out body plethysmography in awake neonates on postnatal days 1, 2, 6, 10, 14, and 18. Data from 12 nicotine-exposed animals were compared with data from 12 saline-exposed animals. Nicotine (6 mg/kg of nicotine tartrate per day) or saline exposure was induced by osmotic minipumps that were implanted subdermally on the fifth day of gestation in Sprague–Dawley Dams. Although both saline- and nicotine-exposed pups gained weight at the same rate throughout the studies, there were subtle differences in ventilatory indices between the two groups. Nicotine-exposed animals had a significantly higher breathing frequency on day 10, and a lower tidal volume on days 14 and 18. Although ventilation tended to be lower in the nicotine-exposed animals, the difference was not significant. There was a significantly higher frequency of apneas in the nicotine-exposed compared with the saline-exposed animals on postnatal days 1 and 2, but the apnea duration did not differ between the groups. No apneas were observed in any of the animals after the sixth postnatal day. Prenatal nicotine exposure is associated with a greater incidence of apneas on the first two postnatal days, and then an altered breathing pattern that manifests at a later stage of development. © 2004 Elsevier B.V. All rights reserved. Keywords: In vivo; Neonatal rat; Respiratory frequency; Plethysmography; Tidal volume 1. Introduction Infants born to mothers that smoke while pregnant have a relatively high incidence of central respiratory control abnormalities (e.g., apnea, delayed arousal re- sponses, diminished chemoreceptor reflexes) (Gennser ∗ Corresponding author. Tel.: +1 520 621 2203; fax: +1 520 621 8170. E-mail address: fregosi@u.arizona.edu (R.F. Fregosi). et al., 1975; Kahn et al., 2002; Lewis and Bosque, 1995; Toubas et al., 1986; Ueda et al., 1999) and are more likely to die from the sudden infant death syn- drome (SIDS) (DiFranza and Lew, 1995; Kinney et al., 1992). Thus, understanding how both acute and chronic nicotine exposure affects the cardiorespiratory system, including its development, is important. In re- cent years, numerous investigators have employed the rat as a model to study this problem at the systems and cellular level. This model is popular because it is easy 1569-9048/$ – see front matter © 2004 Elsevier B.V. All rights reserved. doi:10.1016/j.resp.2004.07.002