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


     


J Appl Physiol 75: 1233-1237, 1993;
8750-7587/93 $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
Right arrow Citation Map
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 Becker, P. M.
Right arrow Articles by Sylvester, J. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Becker, P. M.
Right arrow Articles by Sylvester, J. T.

Journal of Applied Physiology, Vol 75, Issue 3 1233-1237, Copyright © 1993 by American Physiological Society


ARTICLES

Effects of oxygen tension and glucose concentration on ischemic injury in ventilated ferret lungs

P. M. Becker, D. B. Pearse and J. T. Sylvester
Division of Pulmonary and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.

In the ventilated ischemic lung, oxygen tension will increase at a time when glucose depletion may impair antioxidant defenses, thereby predisposing the lung to injury mediated by oxygen radicals. In the unventilated ischemic lung, however, glucose depletion in the setting of low oxygen tension may decrease production of ATP, leading to injury by a different mechanism. In this study, we evaluated the role of both oxygen tension and glucose concentration on ischemic injury in isolated ferret lungs. Injury, defined as an increase in vascular permeability, was assessed by measurement of filtration coefficient (Kf) and osmotic reflection coefficient for albumin (sigma alb) after 3 h of normothermic (37 degrees C) ischemia without reperfusion. Lungs were ventilated with either 95% O2-5% CO2 or 0% O2-5% CO2. The vasculature was flushed with physiological salt solution containing either 15 mM glucose (hyperoxia-glucose, anoxia-glucose), 15 mM sucrose (hyperoxia-sucrose, anoxia-sucrose), or no substrate (hyperoxia-no substrate, anoxia-no substrate) (n = 6 for each condition). Kf and sigma alb in hyperoxia-no substrate group did not differ from values in minimally ischemic normoxic normoglycemic ferret lungs. Without glucose, ischemic injury was worse in anoxic than in hyperoxic lungs. With glucose, ischemic injury was worse in hyperoxic than in anoxic lungs. Glucose exacerbated injury in hyperoxic, but not anoxic, lungs. These results indicate that ischemic injury in these lungs depended on both oxygen tension and glucose concentration and suggest that both oxygen radical generation and ATP depletion during ischemia may contribute to the development of this injury.


This article has been cited by other articles:


Home page
Eur. J. Cardiothorac. Surg.Home page
Y. Lamarche, J. Gagnon, O. Malo, G. Blaise, M. Carrier, and L. P. Perrault
Ventilation prevents pulmonary endothelial dysfunction and improves oxygenation after cardiopulmonary bypass without aortic cross-clamping
Eur. J. Cardiothorac. Surg., September 1, 2004; 26(3): 554 - 563.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
P. M. Becker, A. A. Kazi, R. Wadgaonkar, D. B. Pearse, D. Kwiatkowski, and J. G. N. Garcia
Pulmonary Vascular Permeability and Ischemic Injury in Gelsolin-Deficient Mice
Am. J. Respir. Cell Mol. Biol., April 1, 2003; 28(4): 478 - 484.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
P. M. Becker, A. D. Verin, M. A. Booth, F. Liu, A. Birukova, and J. G. N. Garcia
Differential regulation of diverse physiological responses to VEGF in pulmonary endothelial cells
Am J Physiol Lung Cell Mol Physiol, December 1, 2001; 281(6): L1500 - L1511.
[Abstract] [Full Text] [PDF]


Home page
Eur Respir JHome page
H. Schutte, A. Lockinger, W. Seeger, and F. Grimminger
Aerosolized PGE1, PGI2 and nitroprusside protect against vascular leakage in lung ischaemia-reperfusion
Eur. Respir. J., July 1, 2001; 18(1): 15 - 22.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
P. M. Becker, A. Alcasabas, A. Y. Yu, G. L. Semenza, and T. E. Bunton
Oxygen-Independent Upregulation of Vascular Endothelial Growth Factor and Vascular Barrier Dysfunction during Ventilated Pulmonary Ischemia in Isolated Ferret Lungs
Am. J. Respir. Cell Mol. Biol., March 1, 2000; 22(3): 272 - 279.
[Abstract] [Full Text]


Home page
J. Appl. Physiol.Home page
D. B. Pearse, E. M. Wagner, and S. Permutt
Effect of ventilation on vascular permeability and cyclic nucleotide concentrations in ischemic sheep lungs
J Appl Physiol, January 1, 1999; 86(1): 123 - 132.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
Y. Minamiya, K. Tozawa, M. Kitamura, S. Saito, and J.-i. Ogawa
Platelet-activating Factor Mediates Intercellular Adhesion Molecule-1-dependent Radical Production in the Nonhypoxic Ischemia Rat Lung
Am. J. Respir. Cell Mol. Biol., July 1, 1998; 19(1): 150 - 157.
[Abstract] [Full Text]


Home page
J. Appl. Physiol.Home page
P. M. Becker, W. Buchanan, and J. T. Sylvester
Protective effects of intravascular pressure and nitric oxide in ischemic lung injury
J Appl Physiol, March 1, 1998; 84(3): 803 - 808.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
H. SCHÜTTE, G. HERMLE, W. SEEGER, and F. GRIMMINGER
Vascular Distension and Continued Ventilation Are Protective in Lung Ischemia/Reperfusion
Am. J. Respir. Crit. Care Med., January 1, 1997; 157(1): 171 - 177.
[Abstract] [Full Text]




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