University of Illinois, Medical Department publishes research in angiotensins

   "In the present study, we evaluated the effect of propofol on endotoxin-induced ALI and endothelial dysfunction. 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). 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," wrote E.G. Vottavelis and colleagues, University of Illinois, Medical Department.

   The researchers concluded: "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. (Anesth Analg 2007;105:1363-70)'."

   Vottavelis and colleagues published their study in Anesthesia and Analgesia (Propofol attenuates endotoxin-induced endothelial cell injury, angiotensin-converting enzyme shedding, and lung edema. Anesthesia and Analgesia, 2007;105(5):1363-1370).

   For additional information, contact I.V. Balyasnikova, University of Illinois, Anesthesiology Research Center, College Medical, Dept. of Anesthesiology, 1819 W Polk St. MC 519, Chicago, IL 60612, USA.

   Publisher contact information for the journal Anesthesia and Analgesia is: Lippincott Williams & Wilkins, 530 Walnut St., Philadelphia, PA 19106-3621, USA.

   Keywords: United States, Chicago, Angiotensins, Anesthesia, Angiotensin, Biotechnology, Blood Transfusion, Drugs, Edema, Ischemia, Medical Device, Monoclonal Antibody, Pain Medicine, Perfusion, Pharmaceuticals, Propofol, Reperfusion, Therapy, Transfusion Medicine, Treatment, University of Illinois, Medical Department.

   This article was prepared by Pain & Central Nervous System Week editors from staff and other reports. Copyright 2007, Pain & Central Nervous System Week via NewsRx.com.

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