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Studies on mechanisms of cough augmention in SO_2 -exposed guinea-pigs

Little is known about why coughing augments under the condition of airway diseases. To clarify this, we investigated the property of various inflammatory mediators as cough stimulants in normal and SO_2 -exposed guinea-pigs. 「Methods」 The animal was placed in a plethysmograph and inflammatery mediat...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1993, Vol.61 (suppl.1), p.80-80
Main Authors: Kiyoto Sakata, Kazuo Takahama, Hirofumi Kai, Youichiro Isohama, Ichiro Hamanura, Takeshi Miyata
Format: Article
Language:Japanese
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Summary:Little is known about why coughing augments under the condition of airway diseases. To clarify this, we investigated the property of various inflammatory mediators as cough stimulants in normal and SO_2 -exposed guinea-pigs. 「Methods」 The animal was placed in a plethysmograph and inflammatery mediators were inhaled for 2 min. The degree of airway inflammation in SO_2 -exposed animals was histologically verified. 「Results」 In normal animals, substance P (SP), neurokinin A (NKA) and bradykinin induced coughs at low concentrations of 10^-15 M, 10^-13 M and 10^-14 M, respectively. PGE_2 and PAF ( 10^-8 M) also -induced coughing. While histamine (His) induced at a high concentration of 10^4 M, ACh and LTB_4 did not. In SO_2 -exposed animals, SP-, NKA- and His-induced coughing was significantly augmented and the thresholds for cough production decreased. In histological studies on guinea-pigs exposed to SO_2 for a week, the denudation of tracheal and bronchial epithelial cells and damage to tight junctions were not observed in spite of the injury of cilia in ciliated cells. Migration of neutrophils and lymphocytes were observed around the tracheal and bronchial epithelial cells. The results suggest that several inflammatory mediators stimulate coughing at different thresholds and that the increase in cough responsiveness in guinea-pigs exposed to SO_2 may not be associated with epithelium denudation and damage to tight junction.
ISSN:0021-5198