Eosinophilia induced vascular and airway remodeling and
hyperresponsiveness in rat lungs.
Yoshikawa, Sawako, Stephen G. Kayes, Sherri L. Martin, and James C.
Parker.
Departments of Physiology and Structural/Cellular Biology, College
of Medicine, University of South Alabama, Mobile AL 36688
APStracts 3:0226A, 1996.
We evaluated the effects of pulmonary infiltration of eosinophils
without exogenous activators on airway and vascular
hyperresponsiveness to muscarinic challenge in the lungs of rats
infected with Toxicara canis, the canine round worm. Bronchoalveolar
lavage of infected lungs produced 42.6 million cells with 85%
eosinophils, 15% mononuclear cells and essentially no neutrophils.
Eosinophils were present in the air spaces and interstitial spaces
surrounding both airways and vessels. The smooth muscle thickness
increased about 4-fold in large airways and vessels, and medium and
small vessels were muscularized in infected lungs. Compared to
uninfected control lungs, the T. canis infected lungs had increases
in baseline airway resistance (Raw) of 288%, total vascular
resistance (Rt) of 202% and capillary filtration coefficient (Kf,c)
of 208%. Lung compliance (CL) was 56% of control. The EC50 for
infused acetylcholine for uninfected controls was greater than
infected lungs by 18.4 times for Raw and 18.7 times for Rt.
Isoproterenol (10-4M) decreased Rt and peak airway pressure by 21% in
infected lungs but had no significant effect on controls. We conclude
that pulmonary interstitial infiltrates of eosinophils cause airway
and vascular remodeling and increase baseline resistances and
muscarinic reactivities of both airways and vessels in rat lungs
infected with T. canis.
Received 1 December 1994; accepted in final form 27 March 1996.
APS Manuscript Number A1223-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 May 96