Pulmonary chemoreflex sensitivity is enhanced by prostaglandin e2
in anesthetized rats.
Lee, Lu-Yuan, Robert F. Morton.
Department of Physiology and Biophysics, University of Kentucky,
Lexington, Kentucky, U.S.A.
APStracts 2:0298A, 1995.
Stimulation of vagal pulmonary C-fiber afferents by chemical irritants
is believed to be responsible for eliciting the pulmonary chemoreflex
(apnea, bradycardia and hypotension). This study was carried out in
anesthetized Sprague-Dawley rats to determine whether pulmonary
chemoreflex was altered by prostaglandin E2 (PGE2) which is one of
the major inflammatory mediators in the lungs and known to enhance
the sensitivity of C-fiber afferents in several other organ systems.
Capsaicin injected at a dose just above the stimulation threshold
(0.25 or 0.5 _g/kg, i.v.) elicited a very mild respiratory and
cardiovascular depression. In a sharp contrast, during a constant
infusion of PGE2 (1.5 [mu]g/kg/min, i.v.), the same dose of capsaicin
triggered a long apnea, expiratory duration (TE) reaching 843% of the
baseline TE, accompanied by intense bradycardia and hypotension.
Similarly, pulmonary chemoreflex response elicited by a bolus
injection of phenylbiguanide (PBG, 1 or 2 _g/kg, i.v.) was also
greatly augmented by PGE2. These enhanced responses were completely
abolished by a perineural capsaicin treatment of both cervical vagi
to selectively block the conduction of C-fibers, suggesting the
involvement of these afferents. Electrophysiological recording of
pulmonary C-fiber afferent activity further supported our conclusion
that the sensitivity of these sensory endings to capsaicin challenge
was potentiated by PGE2.
Received 25 April 1995; accepted in final form 20 June 1995.
APS Manuscript Number A443-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.