Effect of human respiratory syncytial virus on nonadrenergic
noncholinergic inhibition in cotton rat airways.
Colasurdo, Giuseppe N., Val G. Hemming, Gregory A. Prince, Joan E.
Loader, Juanita P. Graves, Gary L. Larsen.
Division of Pediatric Pulmonary Medicine, National Jewish Center
for Immunology and Respiratory Medicine, University of Colorado
School of Medicine, Denver, Colorado, and Department of Pediatrics,
Uniformed Services University of the Health Sciences, Bethesda,
Maryland, and Virion Systems, Inc., Rockville, Maryland
APStracts 2:0025L, 1995.
A dysfunction of the nonadrenergic noncholinergic inhibitory (NANCi)
system has been invoked as a possible mechanism underlying or
contributing to altered airway function. In the present study we
assessed whether human respiratory syncytial virus (HRSV) infection
affects the airways' neurally mediated contractile and relaxant
(NANCi) responses in vitro. NANCi responses were studied on tracheal
smooth muscle (TSM) segments obtained from young adult cotton rats, a
well established model for HRSV infection. To assess NANCi responses,
TSM segments were removed and placed in tissue baths containing
modified Krebs-Henseleit, atropine (1x10-6 M) and propranolol (5x10-6
M). After contraction with neurokinin A (1x10-5 M), electrical field
stimulation (EFS) was applied at stimulation frequencies ranging from
5 to 30 Hz. The NANCi responses were measured and expressed as the
mean (+/- SEM) percent relaxation. To evaluate neurally mediated
contractile responses, full frequency response curves (0.5-30 Hz) to
EFS were also performed. We found significantly decreased NANCi
responses in TSM segments obtained from infected cotton rats (n=12)
when compared to control animals (n=9) (p<0.002). Furthermore, the
contractile responses to EFS were increased in infected animals when
compared to the control group (p=0.0001). These findings demonstrate
that HRSV infection leads to an enhanced contractile response to EFS
and a significant decrease in NANCi response in cotton rat airways in
vitro. This disruption of the airways' neural control may lead to the
development of altered airway function.
Received 5 August 1994; accepted in final form 6 February 1995.
APS Manuscript Number L223-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.