Introduction: Although a contributory role for neutrophils is well established, recent evidence suggests lymphocytes, in particular T-cells, can also directly mediate IR injury. We have previously demonstrated in vitro that lymphocyte adhesion can be increased following incubation with activated platelets. This study further investigated lymphocyte and platelet recruitment in vivo in a model of mouse hepatic IR injury using intravital microscopy (IVM). Most intravital studies visualise trafficking of ex vivo labelled donor cells. Since this may underestimate actual numbers of cells recruited, we compared adhesion of exogenously injected platelets and lymphocytes with a ‘novel’ method of labelling these cells endogenously. Methods: Experiments were conducted in anaesthetised mice undergoing hepatic IR injury or sham surgery. To monitor exogenous cells, donor spleen derived T- and B-cells were labelled with CFSE and cell tracker orange respectively and injected via the carotid artery into mice undergoing IVM. To quantitate donor platelet adhesion, CFSE-labelled whole blood platelets were injected in separate mice. To investigate endogenous cell recruitment, T-cells, B-cells and platelets were fluorescently labelled in vivo with anti-CD3/Alexa 647 , anti-CD19/Alexa 488 and anti-CD41/Alexa 555 conjugated antibodies respectively. Results: Adhesion of ex vivo labelled T-cells, but not B-cells, was significantly (p<0.001) increased in IR mice compared to shams, albeit numbers were small (1-2 cells/ 20x field). Although donor platelet numbers were similar in IR and sham mice, they were surprisingly high. A significant (p<0.001) decrease in free flowing platelets was observed indicative of poor hepatic blood flow in IR mice. Endogenous T-cell adhesion also significantly (p<0.001) increased in IR mice but no difference in B-cell or platelet adhesion was observed. However, we found that the fluorescent intravital images of endogenously labelled cells did not differ from those obtained when fluorescently conjugated IgG antibodies were injected. This could be due to hepatic ‘trapping’ of the antibodies. Conclusions: Monitoring donor cells labelled ex vivo with cytoplasmic dyes, rather than conjugated antibody labelled endogenous cells, was a more reliable method for quantitating hepatic cell trafficking. This method demonstrated increased recruitment of T-cells, but not B-cells, following IR injury. Adherent T-cell numbers were small, possibly due to their immediate uptake by the spleen post-infusion. We are currently comparing carotid artery cell infusion to intraportal infusion. Since numerous adherent platelets were observed in the liver, further in vivo studies will be conducted in thrombocytopenic mice to determine whether they mediate T-cell recruitment.