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Ventilatory consequences of acute and chronic exposure to nicotine
Author(s) -
Brundage Cord M,
Buehner Justin C,
Taylor Barbara E
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1444-c
Subject(s) - nicotine , anesthesia , respiratory system , medicine , brainstem , control of respiration , hypercapnia
Developmental nicotine exposure has been associated with depressed respiratory responses to hypoxic and hypercapnic conditions. We investigated the effect that chronic and acute nicotine exposure (CNE and ANE, respectively) had on the attenuation of hypoxic and hypercapnic respiratory drive. We measured neural correlates of ventilation from the facial and hypoglossal nerves of the isolated tadpole ( Rana catesbeiana ) brainstem superfused with artificial cerebrospinal fluid (aCSF). Fictive lung and gill breaths were monitored in response to normoxic/normocapnic conditions as well as in response to hypoxic and hypercapnic conditions. Tadpoles were exposed to nicotine either chronically throughout development (18ng/ml pond water for 10 weeks) or acutely with nicotine superfusion of their brainstem (18ng/ml aCSF for 30 minutes). Both CNE and ANE animals demonstrated neuroventilatory gill ataxia in response to hypoxic and hypercapnic conditions. CNE tadpoles failed to produce a significant fictive lung response to either hypoxic or hypercapnic conditions. There was no significant difference between lung responses among ANE and control animals. This would suggest that duration of nicotine exposure influences how that exposure impacts respiratory drive. Implications in Sudden Infant Death Syndrome are discussed. Funded by NIH‐NINDS 2U54NS041069‐06AI.