Components of the activated complement cascade are considered to play a pivotal role in ischemia reperfusion induced organ injury. Using intravital epifluorescence microscopy we investigated the effect of complement inhibition by the recombinant soluble complement receptor 1 (sCR1, TP10) on the effect of macromolecular microvascular permeability, functional capillary perfusion and leukocyte endothelium interaction in postischemic pancreatitis. Anaesthetised Sprague-Dawley rats were subjected to 60 min of normothermic pancreatic ischemia induced by microclipping of the blood supplying arteries of the organ. Rats who received intravenous sCR1 (15 mg/kg b.w.; n = 7) during reperfusion showed a significant reduction of permeability (1.77 ± 1.34 ^*10^-8 cm/s.; n = 7) of TRITC-Rhodamin labelled albumin injected 90 min after the onset of reperfusion as compared to vehicle treated animals (6.95 ± 1.56 ^*10^-8 cm/s) (n= 7). 120 min after the onset of reperfusion the length of red blood cell perfused capillaries (FCD) was significantly improved (from 279 ± 15.7 cm^-1to 330 ± 3.7 cm^-1.; n = 7) and the number of leukocytes adherent to postcapillary venules was significantly reduced (from 314 ± 87 mm^-2 to 163 ± 71 mm^-2.; n = 7) by sCR1 as compared to vehicle treatment. Complement inhibition by sCR1 ameliorates effectively pancreatic ischemia-reperfusion induced microcirculatory disturbances and might be considered for treatment of postischemic pancreatitis.