Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 75: 1955-1961, 1993;
8750-7587/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lee, L. Y.
Right arrow Articles by Burki, N. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, L. Y.
Right arrow Articles by Burki, N. K.

Journal of Applied Physiology, Vol 75, Issue 5 1955-1961, Copyright © 1993 by American Physiological Society


ARTICLES

Nicotine is responsible for airway irritation evoked by cigarette smoke inhalation in men

L. Y. Lee, D. C. Gerhardstein, A. L. Wang and N. K. Burki
Department of Physiology, University of Kentucky, Lexington 40536-0084.

To determine whether nicotine is involved in evoking the irritant effects of cigarette smoke in airways, we studied the responses to inhalation of a single puff (30 ml) of three types of smoke (high nicotine, low nicotine, and gas phase) in healthy male nonsmokers. After the upper airways were locally anesthetized, the subjects, breathing through a mouthpiece, were instructed to signal the detection and the intensity of airway irritation with a push-button device. Inhalation of high-nicotine smoke consistently triggered an intense airway irritation in the lower neck and upper chest region; the total number of push-button signals generated in the first 5 s was 6.61 +/- 0.87 (mean +/- SE, n = 12), with a detection latency of 0.93 +/- 0.11 s. By contrast, inhalation of low-nicotine and gas phase smoke either was not detected or caused only very mild irritation (0.89 +/- 0.4 and 0.36 +/- 0.22, respectively). In addition, the intensity of smoke-induced airway irritation was markedly reduced after premedication with aerosolized hexamethonium, a nicotinic receptor antagonist (P < 0.01, n = 8). Furthermore, inhalation of nicotine aerosol also immediately evoked intense airway irritation and coughs (n = 5). Thus we conclude that the airway irritation evoked by inhaling cigarette smoke results from an activation of sensory endings located in the central airways and nicotine is the primary agent responsible for this action.


This article has been cited by other articles:


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. Xu, W. Yang, G. Zhang, Q. Gu, and L.-Y. Lee
Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons
Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L54 - L61.
[Abstract] [Full Text] [PDF]


Home page
Chem SensesHome page
H. Alimohammadi and W. L. Silver
Evidence for Nicotinic Acetylcholine Receptors on Nasal Trigeminal Nerve Endings of the Rat
Chem Senses, February 1, 2000; 25(1): 61 - 66.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online