BACKGROUND: @entity647 ( @entity647 ) is a frequent complication in septic @entity1 . Previously, we found that @entity1875 , a highly lipid-soluble anesthetic, @entity63 -reperfusion and oxidative lung injury in the isolated perfused @entity35 lung. In the present study, we evaluated the effect of @entity1875 on endotoxin-induced @entity647 and @entity409 . METHODS: The effect of @entity1875 on endotoxin-induced lung endothelial injury was evaluated by plasma and lung tissue homogenate @entity1811 ( @entity1811 ) activity, pulmonary vascular anti- @entity1811 monoclonal antibody binding, and lung wet weight to body weight ratio (LW/BW). RESULTS: When injected IV into @entity35 , endotoxin produced endothelial cell @entity651 , as indicated by: 1) an increase in plasma @entity1811 activity, 2) a decrease in lung @entity1811 activity and anti- @entity1811 monoclonal antibody binding, and 3) an increase in LW/BW. Monoclonal antibody 1A2 was up to 1.8 times more sensitive than other anti- @entity1811 monoclonal antibodies in detecting the decrease in @entity1811 in lungs of endotoxin-treated @entity35 . Pretreatment of @entity35 with a bolus of @entity1875 before endotoxin injection significantly inhibited the increase in @entity1811 activity in the blood, the decrease in @entity1811 activity in the lung, the decrease in anti- @entity1811 monoclonal antibody binding in the lung, and the increase in LW/BW ratio. Importantly, @entity1875 also significantly increased the survival rate of endotoxin-treated animals. The protective effect of @entity1875 in endotoxin-treated animals in vivo was confirmed in vitro, i.e., @entity1875 decreased endothelial cell injury and @entity1811 shedding from endothelial cells in culture. CONCLUSIONS: These results suggest that @entity1875 offers significant protection against endotoxin-induced pulmonary microvessel endothelial cell injury and that anti- @entity1811 monoclonal antibody 1A2 is a sensitive probe for monitoring @entity409 and @entity647 during @entity295 .

XXXX attenuates endotoxin-induced endothelial cell injury, angiotensin-converting enzyme shedding, and lung edema.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity1811 :: ('24310(Tax:10116)', 'Gene') :: ['angiotensin I converting enzyme', 'ACE'] @entity295 :: ('MESH:D018805', 'Disease') :: ['sepsis'] @entity63 :: ('MESH:D007511', 'Disease') :: ['attenuates ischemia'] @entity409 :: ('MESH:D008107', 'Disease') :: ['endothelial dysfunction'] @entity651 :: ('MESH:D055370', 'Disease') :: ['injury and lung edema'] @entity1875 :: ('MESH:D015742', 'Chemical') :: ['propofol'] @entity35 :: ('10116', 'Species') :: ['rat', 'rats'] @entity647 :: ('MESH:D055371', 'Disease') :: ['ALI', 'Acute lung injury']
@entity1875 :: (MESH:D015742,Chemical) :: ['Propofol']
