TY - JOUR
T1 - Stimulation of vagal pulmonary C-fibers by a single breath of cigarette smoke in dogs
AU - Lee, L. Y.
AU - Kou, Y. R.
AU - Frazier, D. T.
AU - Beck, E. R.
AU - Pisarri, T. E.
AU - Coleridge, H. M.
AU - Coleridge, J. C.G.
PY - 1989
Y1 - 1989
N2 - Inhalation of cigarette smoke into the lower airway via a tracheostomy evokes immediate apnea, bradycardia, and systemic hypotension in dogs. These responses can still be evoked when conduction in myelinated vagal fibers is blocked preferentially by cooling but are abolished by vagotomy, suggesting that they are mediated by afferent vagal C-fibers. To examine this possibility, we recorded impulses in pulmonary C-fibers in anesthetized, open-chest dogs and delivered 120 ml cigarette smoke to the lungs in a single ventilatory cycle. Pulmonary C-fibers were stimulated within 1 or 2 s of the delivery of smoke generated by high-nicotine cigarettes, activity increasing from 0.3 ± 0.1 to a peak of 12.6 ± 1.3 (SE) impulses/s (n = 60); the evoked discharge usually lasted 3-5 s. Smoke generated by low-nicotine cigarettes evoked a milder stimulation in 33% of pulmonary C-fibers but did not significantly affect the overall firing frequency (peak activity = 2.2 ± 1.1 impulses/s, n = 36). Hexamethonium (0.7 - 1.2 mg/kg iv) prevented C-fiber stimulation by high-nicotine cigarette smoke (n = 12) but not stimulation by right atrial injection of capsaicin. We conclude that pulmonary C-fibers are stimulated by a single breath of cigarette smoke and that nicotine is the constituent responsible.
AB - Inhalation of cigarette smoke into the lower airway via a tracheostomy evokes immediate apnea, bradycardia, and systemic hypotension in dogs. These responses can still be evoked when conduction in myelinated vagal fibers is blocked preferentially by cooling but are abolished by vagotomy, suggesting that they are mediated by afferent vagal C-fibers. To examine this possibility, we recorded impulses in pulmonary C-fibers in anesthetized, open-chest dogs and delivered 120 ml cigarette smoke to the lungs in a single ventilatory cycle. Pulmonary C-fibers were stimulated within 1 or 2 s of the delivery of smoke generated by high-nicotine cigarettes, activity increasing from 0.3 ± 0.1 to a peak of 12.6 ± 1.3 (SE) impulses/s (n = 60); the evoked discharge usually lasted 3-5 s. Smoke generated by low-nicotine cigarettes evoked a milder stimulation in 33% of pulmonary C-fibers but did not significantly affect the overall firing frequency (peak activity = 2.2 ± 1.1 impulses/s, n = 36). Hexamethonium (0.7 - 1.2 mg/kg iv) prevented C-fiber stimulation by high-nicotine cigarette smoke (n = 12) but not stimulation by right atrial injection of capsaicin. We conclude that pulmonary C-fibers are stimulated by a single breath of cigarette smoke and that nicotine is the constituent responsible.
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U2 - 10.1152/jappl.1989.66.5.2032
DO - 10.1152/jappl.1989.66.5.2032
M3 - Article
C2 - 2568354
AN - SCOPUS:0024340915
SN - 0161-7567
VL - 66
SP - 2032
EP - 2038
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 5
ER -