Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 68: 228-234, 1990;
8750-7587/90 $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 Ahn, S. Y.
Right arrow Articles by Traber, D. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ahn, S. Y.
Right arrow Articles by Traber, D. L.

Journal of Applied Physiology, Vol 68, Issue 1 228-234, Copyright © 1990 by American Physiological Society

ARTICLES

Effects of allopurinol on smoke inhalation in the ovine model

S. Y. Ahn, K. Sugi, P. Talke, J. L. Theissen, H. A. Linares, L. D. Traber, D. N. Herndon and D. L. Traber
University of Texas Medical Branch, Galveston 77550.

We hypothesized that the pulmonary damage induced by smoke inhalation is the result of ischemic reperfusion injury. We determined the effect of allopurinol (xanthine oxidase inhibitor) on the pulmonary microvascular fluid flux in an ovine model after inhalation of cotton smoke (n = 13) and compared these data with those from untreated similarly smoke-injured (n = 7), as well as sham- (air, n = 9) smoked, animals and sheep given an equivalent dose of CO (n = 7). Smoke injury resulted in an increased lung lymph flow, lymph-to-plasma protein ratio, lung content of polymorphonuclear cells, and extravascular lung water (gravametric), in addition to histological evidence of tissue (pulmonary) edema and destruction. No significant difference was found in these variables between the sheep that were injured with smoke whether or not they were pretreated with allopurinol. The sham-smoked and CO-insufflated animals showed no significant changes in cardiopulmonary function or morphology. We conclude that there are few data to support a role of ischemic reperfusion injury in the pulmonary damage seen after smoke inhalation.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. Boueiz, M. Damarla, and P. M. Hassoun
Xanthine oxidoreductase in respiratory and cardiovascular disorders
Am J Physiol Lung Cell Mol Physiol, May 1, 2008; 294(5): L830 - L840.
[Abstract] [Full Text] [PDF]

Home page
 Pharmacol. Rev.Home page
P. Pacher, A. Nivorozhkin, and C. Szabo
Therapeutic effects of xanthine oxidase inhibitors: renaissance half a century after the discovery of allopurinol.
Pharmacol. Rev., March 1, 2006; 58(1): 87 - 114.
[Abstract] [Full Text] [PDF]

Home page
 PhysiologyHome page
K. Murakami and D. L. Traber
Pathophysiological Basis of Smoke Inhalation Injury
Physiology, June 1, 2003; 18(3): 125 - 129.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
H. Sakurai, F. C. Schmalstieg, L. D. Traber, H. K. Hawkins, and D. L. Traber
Role of L-selectin in physiological manifestations after burn and smoke inhalation injury in sheep
J Appl Physiol, April 1, 1999; 86(4): 1151 - 1159.
[Abstract] [Full Text] [PDF]


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