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CRITICAL CARE AND TRAUMA

Propofol Attenuates Endotoxin-Induced Endothelial Cell Injury, Angiotensin-Converting Enzyme Shedding, and Lung Edema

E. Gina Votta-Velis, MD^*, Richard D. Minshall, PhD^*, David J. Visintine, BA^*, Maricela Castellon, BS^*, and Irina V. Balyasnikova, PhD^*

From the Departments of *Anesthesiology and Pharmacology, University of Illinois College of Medicine, Chicago, Illinois.

Address correspondence and reprint requests to Irina V. Balyasnikova, PhD, Anesthesiology Research Center, University of Illinois at Chicago, 1819 W. Polk St. (M/C 519), Chicago, IL 60612. Address e-mail to irinabal{at}uic.edu., irinabal{at}gmail.com.

BACKGROUND: Acute lung injury (ALI) is a frequent complication in septic patients. Previously, we found that propofol, a highly lipid-soluble anesthetic, attenuates ischemia-reperfusion and oxidative lung injury in the isolated perfused rat lung. In the present study, we evaluated the effect of propofol on endotoxin-induced ALI and endothelial dysfunction.

METHODS: The effect of propofol on endotoxin-induced lung endothelial injury was evaluated by plasma and lung tissue homogenate angiotensin I converting enzyme (ACE) activity, pulmonary vascular anti-ACE monoclonal antibody binding, and lung wet weight to body weight ratio (LW/BW).

RESULTS: When injected IV into rats, endotoxin produced endothelial cell injury and lung edema, as indicated by: 1) an increase in plasma ACE activity, 2) a decrease in lung ACE activity and anti-ACE monoclonal antibody binding, and 3) an increase in LW/BW. Monoclonal antibody 1A2 was up to 1.8 times more sensitive than other anti-ACE monoclonal antibodies in detecting the decrease in ACE in lungs of endotoxin-treated rats. Pretreatment of rats with a bolus of propofol before endotoxin injection significantly inhibited the increase in ACE activity in the blood, the decrease in ACE activity in the lung, the decrease in anti-ACE monoclonal antibody binding in the lung, and the increase in LW/BW ratio. Importantly, propofol also significantly increased the survival rate of endotoxin-treated animals. The protective effect of propofol in endotoxin-treated animals in vivo was confirmed in vitro, i.e., propofol decreased endothelial cell injury and ACE shedding from endothelial cells in culture.

CONCLUSIONS: These results suggest that propofol offers significant protection against endotoxin-induced pulmonary microvessel endothelial cell injury and that anti-ACE monoclonal antibody 1A2 is a sensitive probe for monitoring endothelial dysfunction and ALI during sepsis.

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