Mechanisms of injury in hepatic ischemia/reperfusion injury are poorly
defined, Leukocytes are thought to be important in the final mechanis
m of hepatic damage. We intend to show the time course of abnormal leu
kocyte activity in the liver after ischemia/reperfusion (I/R) injury.
Left lobar hepatic ischemia was induced for 20 min in anesthetized C57
B1-6 mice. Measurements were taken at control, reperfusion, and matchi
ng sham times (no ischemia) of 2, 5, 12, and 24 h. Measurements were t
aken using rhodamine and fluorescein enhanced intravital microscopy. P
ost sinusoidal venules were evaluated for numbers of rolling leukocyte
s, leukocyte saltation, and leukocyte velocity. Data are expressed as
number of rolling leukocytes per 100 mu m venule length (2 min). Stati
stical analysis was by ANOVA. The number of rolling leukocytes at 5, 1
2, and 24 h of reperfusion (p<0.001) was significantly higher than con
trol and sham-operated animals. Leukocyte velocities were significantl
y slower in the 12 h I/R group when compared to sham animals (p< 0.001
). These data show that there are definable and quantifiable changes i
n leukocyte kinetics in the liver after ischemia/reperfusion, These ch
anges, which lasted for 24 h, are likely due to upregulation of variou
s endothelial cell adhesion molecules. Delineation of these mechanisms
may be important in disease states such as shock, sepsis, and hepatic
transplantation.