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CARDIOVASCULAR ANESTHESIA

Propofol Attenuates Lung Endothelial Injury Induced by Ischemia-Reperfusion and Oxidative Stress

Departments of Anesthesiology and Pharmacology, University of Illinois at Chicago, Chicago, Illinois

Address correspondence and reprint requests to Sergei M. Danilov, MD, PhD, Anesthesiology Research Center, University of Illinois at Chicago, 1819 W. Polk St. (M/C 519), Chicago, IL 60612. Address e-mail to danilov{at}uic.edu.

Lung dysfunction after cardiopulmonary bypass and lung transplantation results from oxidant-mediated cellular damage. Previously, we observed the shedding of angiotensin-converting enzyme (ACE) from the endothelial cell surface to be a more sensitive and earlier marker of oxidative lung endothelial injury than lung wet-to-dry weight ratio. The aim of this study was to evaluate the potential of the anesthetic propofol, which has antioxidant properties, to prevent oxidative lung injury by measuring ACE shedding. ACE release from isolated perfused rat lungs increased significantly after ischemia-reperfusion (I/R). Propofol significantly decreased I/R-induced ACE release by 23.4% (P < 0.05). Perfusion with 0.75 mM H₂O₂ also caused ACE release from the lung microvasculature, which was similarly attenuated by propofol. The protective effect of propofol on H₂O₂-induced ACE shedding was confirmed in vitro using Chinese Hamster Ovary cells overexpressing human ACE. Thus, propofol can attenuate oxidative injury of the pulmonary endothelium as detected by ACE shedding in I/R and H₂O₂ models of acute lung injury.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999