Esophageal stimulation by hydrochloric acid causes neurogenic
inflammation in the airways in guinea pigs.
Hamamoto, Junji, Hirotsugu Kohrogi, Osamu Kawano, Hajime Iwagoe,
Kazuhiko Fujii, Nahomi Hirata, and Masayuki Ando.
First Department of Internal Medicine, and the Department of
Laboratory Medicine, Kumamoto University School of Medicine, 1-1-1
Honjo, Kumamoto 860, Japan
APStracts 3:0505A, 1996.
To investigate whether tachykinins are released in the airways by
stimulating the esophagus, we studied the airway plasma extravasation
induced by intraesophageal hydrochloric acid (HCl) in the presence or
absence of neutral endopeptidase inhibitor phosphoramidon and NK-1
receptor antagonist FK888 in anesthetized guinea pigs. The airway
plasma leakage was evaluated by measuring extravasated Evans blue dye
in the animals pretreated with propranolol and atropine. One normal
(1 N) HCl infusion into the esophagus significantly increased plasma
extravasation in the trachea. Phosphoramidon significantly
potentiated plasma extravasation in the trachea and main bronchi,
while FK888 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
by intraesophageal HCl stimulation, and 2) there are neural pathways
communicating between the esophagus and airways including the vagus
nerve.
Received 17 July 1996; accepted in final form 29 October 1996.
APS Manuscript Number A676-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996