| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
TRANSLATIONAL PHYSIOLOGY
1Department of Anaesthetics and Intensive Care, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London; and 2Department of Cardiothoracic Surgery and Anaesthetics, Imperial College London, and Heart Science Centre, Harefield Hospital, Harefield, United Kingdom
Submitted 2 December 2004 ; accepted in final form 22 January 2005
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are major causes of morbidity and mortality in the intensive care unit, but despite continuing research few effective therapies have been identified. In recent years, inhaled carbon monoxide (CO) has been reported to have cytoprotective effects in several animal models of tissue injury. We therefore evaluated the effects of inhaled CO in three different in vivo mouse models of ALI. Anesthetized C57BL/6 mice were ventilated with oxygen in the presence or absence of CO (500 parts per million) for 1 h before lung injury was induced by lipopolysaccharide (LPS) or oleic acid (OA) administration. Ventilation was then continued with the same gases for a further 2–3 h, with hemodynamic and respiratory parameters monitored throughout. Intratracheal LPS administration induced lung injury with alveolar inflammation (increased lavage fluid neutrophils, total protein, and cytokines). In contrast, intravenous LPS induced a predominantly vascular lung injury, with increased plasma TNF and increased neutrophil activation (surface Mac-1 upregulation and L-selectin shedding) and sequestration within the pulmonary vasculature. Intravenous OA produced deteriorations in lung function, reflected by changes in respiratory mechanics and blood gases and lavage fluid neutrophil accumulation. However, addition of CO to the inspired gas did not produce significant changes in the measured physiological or immunological parameters in the mouse models used in this study. Thus the results do not support the hypothesis that use of inhaled CO is beneficial in the treatment of ALI and ARDS.
cytokines; lipopolysaccharide; oleic acid; neutrophil recruitment; pulmonary inflammation
This article has been cited by other articles:
|
|
 |
|
  J. A. Nemzek, C. Fry, and O. Abatan Low-dose carbon monoxide treatment attenuates early pulmonary neutrophil recruitment after acid aspiration Am J Physiol Lung Cell Mol Physiol, April 1, 2008; 294(4): L644 - L653. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. R. Wilson, M. E. Goddard, K. P. O'Dea, S. Choudhury, and M. Takata Differential roles of p55 and p75 tumor necrosis factor receptors on stretch-induced pulmonary edema in mice Am J Physiol Lung Cell Mol Physiol, July 1, 2007; 293(1): L60 - L68. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Y. Suh, Y. Jin, A.-K. Yi, X. M. Wang, and A. M. K. Choi CCAAT/Enhancer-Binding Protein Mediates Carbon Monoxide-Induced Suppression of Cyclooxygenase-2 Am. J. Respir. Cell Mol. Biol., August 1, 2006; 35(2): 220 - 226. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. P. O'Dea, A. J. Young, H. Yamamoto, J. L. Robotham, F. M. Brennan, and M. Takata Lung-marginated Monocytes Modulate Pulmonary Microvascular Injury during Early Endotoxemia Am. J. Respir. Crit. Care Med., November 1, 2005; 172(9): 1119 - 1127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Jin and A. M. K. Choi Cytoprotection of Heme Oxygenase-1/Carbon Monoxide in Lung Injury Proceedings of the ATS, October 1, 2005; 2(3): 232 - 235. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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 | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
