Ischemia-reperfusion injury (IRI) leads to increased leukocyte adherence enhancing microvascular dysfunction and acute cellular rejection. ATGs are employed as inductors of immunosupression and represent an option in the treatment of acute cellular rejection but little is known about their effects on the endothelium and the microcirculation after IRI. In a perfusion system isolated extremities (n=60) of 19 cynomolgus monkeys were perfused with three different ATGs after 60 minutes of cold ischemia. ATGs were administered to human blood 30 minutes prior to reperfusion. Using intravital fluorescence microscopy the post-reperfusion microcirculation of skeletal muscle was visualised. Muscle infiltration assessed by immunohistochemistry. Statistical analysis was performed with ANOVA. Significant differences were found between ATG-treated (n=15 x three groups) and ATG-free (n=15) groups. ATGs reduced blood flow impairment (ATG-free: 0.62mm/s; ATG-1: 0.8mm/s, ATG2: 0.82mm/s and ATG3: 1.04mm/s). The number of circulating leukocytes was reduced in the control group in comparison to the ATGgroups (55% Vs. 90%, 82%, 77% respectively). Muscle infiltration is significantly reduced in the ATG-groups. ATGs have a favourable impact on early mechanisms of IRI. Due to reduced leukocyte adherence to the antigen-presenting endothelial cells, recognition vents cannot take place in the post-transplant period of reperfusion. Increase of post-transplant blood flow supports the use of ATGs as pre-transplant induction therapy.