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.
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Fang, LB., Morton, R.F., Wang, A.L. et al. Bronchoconstriction and delayed rapid shallow breathing induced by cigarette smoke inhalation in anesthetized rats. Lung 169, 153–164 (1991). https://doi.org/10.1007/BF02714151
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DOI: https://doi.org/10.1007/BF02714151