Hemorrhagic shock (HS) and resuscitation can be seen as a global body ische
mia-reperfusion (I/R) injury characterized by neutrophil infiltration and o
rgan damage. Liver dysfunction occurs early after HS. Adhesion molecules ar
e needed for the first steps of neutrophil migration. Thus, the purpose of
this study was to investigate the role of L-selectin in the liver after unc
ontrolled HS and resuscitation. Forty-eight Sprague Dawley rats were subjec
ted to uncontrolled HS and resuscitation. Animals were divided into three g
roups: sham, uncontrolled HS and resuscitation, and uncontrolled HS and res
uscitation with anti-1-selectin treatment. At 6 we evaluated liver injury t
ests, liver tissue myeloperoxidase (MPO), and liver histology. Survival was
followed for 3 days and compared between groups. Statistical analysis incl
uded Fisher's exact test and one-way analysis of variance. Survival signifi
cantly increased from 30% in the control group to 60% in the treated group
(p < .05). Hepatocellular and structural injury as well as neutrophil infil
tration was significantly decreased in treated animals (p < .05). Thus, blo
ckade of L-selectin resulted in decreased hepatocellular injury and increas
ed survival in our model of uncontrolled HS. Selectins may be important the
rapeutic targets for blockade in the treatment of HS.