Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 81: 1279-1287, 1996;
8750-7587/96 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoshikawa, S.
Right arrow Articles by Parker, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoshikawa, S.
Right arrow Articles by Parker, J. C.

Journal of Applied Physiology, Vol 81, Issue 3 1279-1287, Copyright © 1996 by American Physiological Society

ARTICLES

Eosinophilia-induced vascular and airway remodeling and hyperresponsiveness in rat lungs

S. Yoshikawa, S. G. Kayes, S. L. Martin and J. C. Parker
Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688, USA.

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 Toxocara [correction of Toxicara] canis, the canine round worm. Bronchoalveolar lavage of infected lungs produced 4.26 x 10(7) cells with 85% eosinophils, 15% mononuclear cells, and essentially no neutrophils. Eosinophils were present in the air spaces and interstitial spaces surrounding airways and vessels. The smooth muscle thickness increased about fourfold in large airways and vessels, and medium and small vessels were muscularized in infected lungs. In the T. canis-infected lungs, baseline airway resistance increased 288%, total vascular resistance (RT) increased 202%, and capillary filtration coefficient increased 208% compared with uninfected control lungs. Lung compliance was 56% of control. The concentration of acetylcholine that produced 50% of maximal response was 18.4 times greater for airway resistance and 18.7 times greater for RT in uninfected controls than in infected lungs. Isoproterenol (10(-4) M) 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 airways and vessels in rat lungs infected with T. canis.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
M. I. Townsley, K. S. Snell, C. L. Ivey, D. E. Culberson, D. C. Liu, R. K. Reed, and O. Mathieu-Costello
Remodeling of lung interstitium but not resistance vessels in canine pacing-induced heart failure
J Appl Physiol, November 1, 1999; 87(5): 1823 - 1830.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. C. Parker, E. C. Breen, and J. B. West
High vascular and airway pressures increase interstitial protein mRNA expression in isolated rat lungs
J Appl Physiol, November 1, 1997; 83(5): 1697 - 1705.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online