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


     

J Appl Physiol 56: 900-905, 1984;
8750-7587/84 $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 Burghuber, O.
Right arrow Articles by Voelkel, N. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Burghuber, O.
Right arrow Articles by Voelkel, N. F.

Journal of Applied Physiology, Vol 56, Issue 4 900-905, Copyright © 1984 by American Physiological Society

ARTICLES

Lung edema due to hydrogen peroxide is independent of cyclooxygenase products

O. Burghuber, M. M. Mathias, I. F. McMurtry, J. T. Reeves and N. F. Voelkel

Active oxygen species can cause lung injury. Although a direct action on endothelial cells is proposed, the possibility exists that they might cause injury via mediators. We considered that active oxygen species would stimulate the generation of cyclooxygenase metabolites, which then alter pulmonary vasoreactivity and cause edema. We chemically produced hydrogen peroxide by adding glucose oxidase to a plasma- and cell-free, but beta-D-glucose-containing, solution, which perfused isolated rat lungs. Addition of glucose oxidase to the perfusate caused a marked decrease in pulmonary vasoreactivity, accompanied by an increase in the concentrations of prostacyclin, thromboxane A2, and prostaglandin F2 alpha. Pretreatment with catalase, a specific scavenger of hydrogen peroxide, preserved pulmonary vasoreactivity, inhibited the increase of the concentration of the measured prostaglandins, and prevented edema formation. Indomethacin effectively blocked lung prostaglandin production but neither prevented the decrease in vasoreactivity nor inhibited edema formation. From these data we conclude that hydrogen peroxide impaired pulmonary vasoreactivity and subsequently caused edema. Despite the fact that hydrogen peroxide stimulated lung prostaglandin production, cyclooxygenase-derived products neither caused the decrease in vasoreactivity nor the development of edema.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
R. Moudgil, E. D. Michelakis, and S. L. Archer
Hypoxic pulmonary vasoconstriction
J Appl Physiol, January 1, 2005; 98(1): 390 - 403.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. L. Archer, V. Hampl, D. P. Nelson, E. Sidney, D. A. Peterson, and E. K. Weir
Dithionite Increases Radical Formation and Decreases Vasoconstriction in the Lung : Evidence That Dithionite Does Not Mimic Alveolar Hypoxia
Circ. Res., July 1, 1995; 77(1): 174 - 181.
[Abstract] [Full Text]

Home page
 ANGIOLOGYHome page
H. Ide, T. Ino, T. Hasegawa, and H. Matsumoto
The Role of Leukocyte Depletion by in Vivo Use of Leukocyte Filter in Lung Preservation After Warm Ischemia
Angiology, April 1, 1990; 41(4): 318 - 327.
[Abstract] [PDF]


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