Introduction 1 2 1 5 1 3 5 6 7 8 The aim of this study was to investigate platelet activation and function in experimental AP. Materials and Methods Animals Monitoring blood samples Animal models −1 −1 −1 −1 9 −1 −1 Platelet preparation 10 Intravital microscopy Erythrocyte and leukocyte assessment 11 12 Platelet assessment Off-line analysis 13 Edema Histology 9 Assessment of thromboxane A2 Statistical analysis t p Results Serum amylase 1 Table 1 Serum Parameters, Wet–Dry Ratio, and Histopathology   Control Mild AP Severe AP Serum parameters Amylase (U/l) 586 ± 116 27,200 ± 4,012* 27,317 ± 3,220* Thromboxane A2 [pg/50 μl] 15.3 ± 10.3 47.8 ± 12.1* 61.9 ± 15.8* Wet–dry ratio 2.87 ± 0.79 6.96 ± 0.95* 4.77 ± 0.70 Histopathology Inflammation 0.25 ± 0.42 1.31 ± 0.08* 1.95 ± 0.17*† Necrosis 0.08 ± 0.20 1.10 ± 0.11* 1.70 ± 0.23*† p † p Serum thromboxane A2 1 Intravital microscopy 2 2 1 2 1 2 Table 2 Results of the Intravital Microscopy Intravital microscopy Control Mild AP Severe AP Erythrocyte velocity (capillary) (mm/s) 0.65/0.02 0.42/0.01* 0.36/0.01* Erythrocyte velocity (venule) (mm/s) 0.93/0.11 0.77/0.17 0.58/0.10*† Platelet velocity (capillary) (mm/s) 0.54 ± 0.04 0.35 ± 0.03* 0.29 ± 0.03* Platelet velocity (venule) (mm/s) 0.67 ± 0.05 0.63 ± 0.02 0.53 ± 0.05* Rolling leukocytes (capillary) 1.3 ± 0.2 4.5 ± 1.4* 9.0 ± 1.7*† Rolling leukocytes (venule) 1.3 ± 0.2 14.8 ± 1.2* 18.9 ± 1.9* Sticking leukocytes (capillary) 1.1 ± 0.3 10.2 ± 1.8* 7.2 ± 0.7* Sticking leukocytes (venule) 0.7 ± 0.1 5.6 ± 0.9* 13.5 ± 2.0*† p p Figure 1 gray white striped left columns right columns p p  Figure 2 gray white striped left columns right columns p p  Tissue edema (wet/dry ratio) 1 Histopathology 1 Discussion 9 14 15 10 15 Acute pancreatitis is characterized by an impairment of microcirculation due to an activation of inflammatory cells with a consecutive increase of leukocyte–endothelium interaction. These pathophysiological events mediate an inflammatory tissue infiltration, edema, and hemorrhagic lesions. While the inflammatory response is well investigated, the platelet function and the role of the coagulation cascade have not yet been investigated in detail. 16 17 18 19 15 20 21 22 23 24 26 18 19 25 26 27 29 Conclusion The results of the present study show that activation and adhesion of platelets play an important role during AP. Platelet–endothelium and platelet–leukocyte interactions as well as thromboxane liberation show a correlation with the severity of experimental AP and seem to be of distinct importance in the progression from mild to severe necrotizing AP. A possible therapeutic use of these pathophysiological events should be evaluated in further studies.