Abstract
Bronchomotor and ventilatory responses to inhalation of cigarette smoke (50% concentration, 6 ml) were studied in anesthetized and vagotomized Sprague-Dawley rats. Low-nicotine cigarette smoke did not cause any detectable delayed response, whereas high-nicotine cigarette smoke induced rapid, shallow breathing, and a marked increase in airway resistance (RL). The increase in f reached a peak (Δf=43±8%) at the 5th breath after the onset of smoke inhalation, preceding both the decrease in VT (ΔVT=-27±4%) and the increase in RL (ΔRL=89±19%); the latter 2 reached their peaks at approximately the 10th breath, displaying a similar temporal pattern of responses between them. The bronchomotor response to high-nicotine cigarette smoke was slightly attenuated but not prevented by prior administration of isoproterenol (0.2 mg/kg, intravenously [iv]), nor was the smoke-induced rapid, shallow breathing. In contrast, prior administration of mecamylamine (0.9 mg/kg, iv) completely abolished both the bronchomotor and ventilatory responses to smoke inhalation, indicating that nicotine is the primary causative agent responsible for these changes.
Original language | English |
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Pages (from-to) | 153-164 |
Number of pages | 12 |
Journal | Lung |
Volume | 169 |
Issue number | 1 |
DOIs | |
State | Published - Dec 1991 |
Keywords
- Airway reflexes
- Bronchomotor tone
- Isoproterenol
- Mecamylamine
- Nicotine
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine