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Background: Acute pancreatitis (AP) is characterized by a disturbance of pancreatic microcirculation, leading to ischemia and consequently necrosis of pancreatic tissue. Leukocyte activation and erythrocyte flow patterns have been well investigated during these pathophysiological processes. In contrast, it remains unclear how platelets contribute to these perfusion disturbances. Aim of our study was to investigate platelet activation and function in experimental models of AP. Methods: AP of graded severity was induced in rats. 1) control animals (n = 6) Ringer’s solution i.V.; 2) mild AP (n=12) cerulein i.V.; 3) severe AP (n=12) glycodeoxycholic acid 2,5 mM intraductal + cerulein i.v. 12 h after induction of AP intravital microscopy was performed in 6 animals of each group after separation and staining of platelets (1 ml blood, rhodamin 6G). Platelet velocity and adhesion to the endothelium was investigated in capillaries and venules. In addition, serum thromboxane B2 levels were measured. In the other 6 animals per group, histology was evaluated 24 h after induction of AP. Results: Histology after 24 h showed a mild AP in cerulein animals. In contrast, in animals with GDOC application, inflammation and necrosis were significantly more evident (inflammation 1,3 ± 0,18 vs. 1,9 ± 0,21, necrosis 1,20 ± 0,11 vs. 1,80 ± 0,28). Intravital microscopy showed significantly more platelet-endothelium interaction in animals with AP compared to control animals (Tabelle 1). Tabelle 1. V kap [mm/s] Roller ven Sticker ven TBXB2[pg/50μl] Control 0,95±0,23 3,2±0,9 0,9±0,5 15,3±10,3 Mild Ap 0,78±0,31 9,2±1,7* 1,2±0,4 47,8±12,1* Severe AP 0,28±0,12* 11,0±1,8* 3,5±0,6* 61,9±15,8* * p > 0,05 vs. control