ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
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 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 Menaouar, A
Right arrow Articles by Grimbert, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Menaouar, A
Right arrow Articles by Grimbert, F.
Eur Respir J 1997; 10: 1100-1107
Copyright © ERS Journals Ltd 1997

Original Articles

Chlorine gas induced acute lung injury in isolated rabbit lung

A Menaouar, D Anglade, P Baussand, A Pelloux, M Corboz, S Lantuejoul, G Benchetrit, and FA Grimbert

This study was designed to investigate the pathogenesis of chlorine gas (Cl2) induced acute lung injury and oedema. Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl2 (n=7) for 10 min. Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl2-exposed lungs, the fluid filtration rate increased from -0.228+/-0.25 to 1.823+/-1.23 mL min(-1) x 100 g(-1) (p<0.001) and the filtration coefficient increased from 0.091+/-0.01 to 0.259+/-0.07 mL x min(-1) x cmH2O(-1) x 100 g(-1) (p<0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6+/-1.6 in the Cl2 group and 4.0+/-0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid. Although the alveolar flooding by oedema is explained, in part, by the Cl2-induced epithelial injury, our results suggest that Cl2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.


This article has been cited by other articles:


Home page
 Canadian J. AnesthesiaHome page
D. Bracco, M.-J. Dubois, and R. Bouali
Intoxication by bleach ingestion
Can J Anesth, January 1, 2005; 52(1): 118 - 119.
[Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
J. G. Martin, H. R. Campbell, H. Iijima, D. Gautrin, J.-L. Malo, D. H. Eidelman, Q. Hamid, and K. Maghni
Chlorine-induced Injury to the Airways in Mice
Am. J. Respir. Crit. Care Med., September 1, 2003; 168(5): 568 - 574.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Chem.Home page
S. A. Jortani, J. W. Snyder, and R. Valdes Jr
The Role of the Clinical Laboratory in Managing Chemical or Biological Terrorism
Clin. Chem., December 1, 2000; 46(12): 1883 - 1893.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
S. BAYAT, A. MENAOUAR, D. ANGLADE, H. ETTINGER, A. FRANCOIS-JOUBERT, G. BENCHETRIT, and F. A. GRIMBERT
In Vivo Quantitation of Epithelial Lining Fluid in Dog Lung
Am. J. Respir. Crit. Care Med., December 1, 1998; 158(6): 1715 - 1723.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the European Respiratory Society.