L-Selectin Blockade and Liver Function in Rats After Uncontrolled Hemorrhagic Shock

Abstract

Hemorrhagic shock (HS) and resuscitation can be seen as a global body ischemia-reperfusion (I/R) injury characterized by neutrophil infiltration and organ damage. Liver dysfunction occurs early after HS. Adhesion molecules are needed for the first steps of neutrophil migration. Thus, the purpose of this study was to investigate the role of -selectin in the liver after uncontrolled HS and resuscitation. Forty-eight L Sprague Dawley rats were subjected to uncontrolled HS and resuscitation. Animals were divided into three groups: sham, uncontrolled HS and resuscitation, and uncontrolled HS and resuscitation with anti--selectin L treatment. At 6 we evaluated liver injury tests, liver tissue myeloperoxidase (MPO), and liver histology. Survival was followed for 3 days and compared between groups. Statistical analysis included Fisher's exact test and one-way analysis of variance. Survival significantly increased from 30% in the control group to 60% in the treated group (p < .05). Hepatocellular and structural injury as well as neutrophil infiltration was significantly decreased in treated animals (p < .05). Thus, blockade of -selectin resulted in decreased hepatocellular injury and increased surL vival in our model of uncontrolled HS. Selectins may be important therapeutic targets for blockade in the treatment of HS.

• Ischemia-REPERFUSION Liver L-SELECTIN Uncontrolled Hemorrhagic Shock