help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by GUST, R.
Right arrow Articles by SCHUSTER, D. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by GUST, R.
Right arrow Articles by SCHUSTER, D. P.

Am. J. Respir. Crit. Care Med., Volume 160, Number 4, October 1999, 1165-1170

Role of Cyclooxygenase-2 in Oleic Acid-Induced Acute Lung Injury

RENÉ GUST, JAMES K. KOZLOWSKI, ALAN H. STEPHENSON, and DANIEL P. SCHUSTER

Pulmonary and Critical Care Division, Washington University School of Medicine, St. Louis; and Department of Pharmacological and Physiological Science, St. Louis University School of Medicine, St. Louis, Missouri

Eicosanoid production appears to be important to both edemagenesis and the pattern of pulmonary perfusion in experimental acute lung injury (ALI). We hypothesized that these effects could be mediated by the inducible form of cyclooxygenase (COX-2). We used positron emission tomography to evaluate the pulmonary perfusion pattern in dogs given oleic acid (OA) only (n = 6), the novel COX-2 inhibitor SC-236 50 min before OA (n = 3), and SC-236 given 20 min before endotoxin (Etx), followed by OA given 30 min after Etx (n = 5). Thromboxane B2 (TXB2) and prostacyclin (6-keto prostaglandin F1alpha ; 6-keto PGF1alpha ) metabolite concentrations in plasma and lung tissue were measured in these groups and in another group given Etx + OA (n = 4). Inhibition of COX-2 before administration of OA alone or before administration of Etx and OA did not have any significant effect on plasma or lung tissue concentrations of TXB2. However, inhibition of COX-2 prior to Etx and OA significantly reduced the plasma and lung tissue concentrations of 6-keto PGF1alpha as compared with those in the group given only Etx + OA. Moreover, SC-236 prevented the expected loss of perfusion redistribution associated with Etx + OA only. The effect of endotoxin on pulmonary perfusion in ALI is therefore the result of a COX-2-mediated increase in prostacyclin production in lung tissue.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
G. Y. Park and J. W. Christman
Involvement of cyclooxygenase-2 and prostaglandins in the molecular pathogenesis of inflammatory lung diseases
Am J Physiol Lung Cell Mol Physiol, May 1, 2006; 290(5): L797 - L805.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
S.-F. Ma, D. N. Grigoryev, A. D. Taylor, S. Nonas, S. Sammani, S. Q. Ye, and J. G. N. Garcia
Bioinformatic identification of novel early stress response genes in rodent models of lung injury
Am J Physiol Lung Cell Mol Physiol, September 1, 2005; 289(3): L468 - L477.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
Z. Zhou, J. Kozlowski, and D. P. Schuster
Physiologic, Biochemical, and Imaging Characterization of Acute Lung Injury in Mice
Am. J. Respir. Crit. Care Med., August 1, 2005; 172(3): 344 - 351.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
C. D. Fike, M. R. Kaplowitz, Y. Zhang, and S. L. Pfister
Cyclooxygenase-2 and an early stage of chronic hypoxia-induced pulmonary hypertension in newborn pigs
J Appl Physiol, March 1, 2005; 98(3): 1111 - 1118.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
T. Geiser
The Role of Neutrophils and Neutrophil Products in Pulmonary Hemodynamics of Endotoxin in Oleic Acid-Induced Lung Injury
Anesth. Analg., February 1, 2004; 98(2): 281 - 282.
[Full Text] [PDF]

Home page
 Anesth. Analg.Home page
L. L. Hill, D. L. Chen, J. Kozlowski, and D. P. Schuster
Neutrophils and Neutrophil Products Do Not Mediate Pulmonary Hemodynamic Effects of Endotoxin on Oleic Acid-Induced Lung Injury
Anesth. Analg., February 1, 2004; 98(2): 452 - 457.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
M. Gama de Abreu, M. Heintz, A. Heller, R. Szechenyi, D. M. Albrecht, and T. Koch
One-Lung Ventilation with High Tidal Volumes and Zero Positive End-Expiratory Pressure Is Injurious in the Isolated Rabbit Lung Model
Anesth. Analg., January 1, 2003; 96(1): 220 - 228.
[Abstract] [Full Text] [PDF]

Home page
 JNMHome page
D. P. Schuster, C. Anderson, J. Kozlowski, and N. Lange
Regional Pulmonary Perfusion in Patients with Acute Pulmonary Edema
J. Nucl. Med., July 1, 2002; 43(7): 863 - 870.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D. P. Schuster, J. K. Kozlowski, T. McCarthy, J. Morrow, and A. Stephenson
Effect of endotoxin on oleic acid lung injury does not depend on priming
J Appl Physiol, November 1, 2001; 91(5): 2047 - 2054.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
C. Martin, A. Wohlsen, and S. Uhlig
Changes in airway resistance by simultaneous exposure to TNF-{alpha} and IL-1{beta} in perfused rat lungs
Am J Physiol Lung Cell Mol Physiol, April 1, 2001; 280(4): L595 - L601.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1999 American Thoracic Society 		  SOTA, FL