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1 First Department of Internal Medicine and 2 Department of Laboratory Medicine, Kumamoto University School of Medicine, Kumamoto 860, Japan
Received 17 July 1996; accepted in final form 29 October 1996.
Hamamoto, Junji, Hirotsugu Kohrogi, Osamu Kawano,
Hajime Iwagoe, Kazuhiko Fujii, Nahomi Hirata, and Masayuki Ando.
Esophageal stimulation by hydrochloric acid causes neurogenic
inflammation in the airways in guinea pigs. J. Appl.
Physiol. 82(3): 738-745, 1997.
To
investigate whether tachykinins are released in the airways in response
to stimulation of the esophagus, we studied the airway plasma
extravasation induced by intraesophageal HCl in the presence or absence
of neutral endopeptidase inhibitor phosphoramidon and NK1-receptor antagonist FK-888 in
anesthetized guinea pigs. The airway plasma leakage was
evaluated by measuring extravasated Evans blue dye in the animals
pretreated with propranolol and atropine. Infusion of 1 N HCl into the
esophagus significantly increased plasma extravasation in the trachea.
Phosphoramidon significantly potentiated plasma extravasation in the
trachea and main bronchi, whereas FK-888 significantly inhibited that extravasation in a dose-related manner. In the capsaicin-treated animals, airway plasma extravasation was completely inhibited even in
the presence of phosphoramidon. Tracheal plasma extravasation potentiated by phosphoramidon was significantly inhibited in the bilateral vagotomized animals. These results suggest that
1) tachykinin-like substances are
released to cause plasma extravasation in the airways as a result of
intraesophageal HCl stimulation and
2) there are neural pathways
communicating between the esophagus and airways, including the vagus
nerve.
asthma; tachykinins; cough; esophageal reflux; axon reflex
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