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Research Article Free access | 10.1172/JCI105671
Cardiovascular Research Institute and the Department of Medicine, University of California San Francisco Medical Center, San Francisco, California
‡International Postdoctoral Research Fellow of the U. S. Public Health Service (FO5TW-893).
§U. S. Public Health Service Fellowship HE-24,549.
ǁAddress requests for reprints to Dr. J. A. Nadel, Cardiovascular Research Institute, University of California San Francisco Medical Center, San Francisco, Calif. 94122.
*Received for publication 19 May 1967 and in revised form 12 July 1967.
Supported in part by U. S. Public Health Service grant HE-06285 and by The Swedish Association against Heart and Lung Diseases.
Presented in part at the 9th Aspen Emphysema Conference, 9 June 1966.
Find articles by Simonsson, B. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute and the Department of Medicine, University of California San Francisco Medical Center, San Francisco, California
‡International Postdoctoral Research Fellow of the U. S. Public Health Service (FO5TW-893).
§U. S. Public Health Service Fellowship HE-24,549.
ǁAddress requests for reprints to Dr. J. A. Nadel, Cardiovascular Research Institute, University of California San Francisco Medical Center, San Francisco, Calif. 94122.
*Received for publication 19 May 1967 and in revised form 12 July 1967.
Supported in part by U. S. Public Health Service grant HE-06285 and by The Swedish Association against Heart and Lung Diseases.
Presented in part at the 9th Aspen Emphysema Conference, 9 June 1966.
Find articles by Jacobs, F. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute and the Department of Medicine, University of California San Francisco Medical Center, San Francisco, California
‡International Postdoctoral Research Fellow of the U. S. Public Health Service (FO5TW-893).
§U. S. Public Health Service Fellowship HE-24,549.
ǁAddress requests for reprints to Dr. J. A. Nadel, Cardiovascular Research Institute, University of California San Francisco Medical Center, San Francisco, Calif. 94122.
*Received for publication 19 May 1967 and in revised form 12 July 1967.
Supported in part by U. S. Public Health Service grant HE-06285 and by The Swedish Association against Heart and Lung Diseases.
Presented in part at the 9th Aspen Emphysema Conference, 9 June 1966.
Find articles by Nadel, J. in: JCI | PubMed | Google Scholar
Published November 1, 1967 - More info
Inhalation of aerosols of citric acid, histamine phosphate, or carbon dust, or air cooled to - 20°C or rapid respiratory maneuvers (inspiration or expiration) results in an increase in airway resistance in some patients with asthma or bronchitis. It has been shown previously in animals that stimulation of cough receptors results in bronchoconstriction through efferent cholinergic pathways. In the patients studied, the administration of atropine sulfate, which would block such pathways, abolished the bronchoconstrictor effects of all the stimuli except large doses of histamine, which may exert a direct effect on airway smooth muscle. These data suggest that sensitized cough receptors may be involved in triggering reflex airway constriction in such patients.