Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2847751 | Respiratory Physiology & Neurobiology | 2009 | 5 Pages |
Intermittent hypoxia can evoke persistent increases in ventilation (V˙E) in neonates (i.e. long-term facilitation, LTF) (Julien et al., 2008). Since prenatal nicotine (PN) exposure alters neonatal respiratory control (Fregosi and Pilarski, 2008), we hypothesized that PN would influence LTF of ventilation (V˙E) in neonatal rats. An osmotic minipump delivered nicotine 6 mg/kg per day or saline to pregnant dams. V˙E was assessed in unanesthetized pups via whole body plethysmography at post-natal (P) days 9–11 or 15–17 during baseline (BL, 21% O2), hypoxia (10 × 5 min, 5% O2) and 30 min post-hypoxia. PN pups had reduced BL V˙E (p < 0.05) but greater increases in V˙E during hypoxia (p < 0.05). Post-hypoxia V˙E (i.e. LTF) showed an age × treatment interaction (p < 0.01) with similar values at P9–11 but enhanced LTF in saline (30 ± 8%BL) vs. PN pups (6 ± 5%BL; p = 0.01) at P15–17. We conclude that the post-natal developmental time course of hypoxia-induced LTF is influenced by PN.