Objective: To set up a swine model of severe acute pancreatitis(SAP) and to observe its relationship with the gut-originated bacteria/endotoxin translocation. Methods: Forty pigs weighing 17-22 kg were randomly divided into SAP group (n= 34) and sham-SAP group(n= 6). By injecting 1 ml/kg of com bined solution of 5% sodium taurocholate and 8 000-10 000 benzoyl arginine ethyl ester (BAEE) units trypsin per milliliter into pancreas via pancreatic duct, SAP was induced under anesthesia. Endotoxin samples from vena cava were determined by chromogenic limulus amebocyte lysate (LAL) technique. Both portal and central vena blood samples were collected before and 72 h after the induction of SAP and cultured for both aerobic and anaerobic bacterial growth. Animals were sacrificed at the end of experiments by injecting 20 ml of 10% KC1 intravenously and tissue specimens of mesenteriolum and mesocolon lymph nodes, lung, pulmonary portal lymph nods and pancreas were taken immediately after animal death, and homogenized for bacteriological studies. Results: Systemic plasma endotoxin levels increased rapidly 6 h post induction of SAP(PIS) with a peak at 48 h PIS (P＜0.01). The magnitude of bacterial translocation in both portal and systemic blood and remote systemic organs as well were recovered PIS. Conclusion:(1)A swine model of SAP was established; (2)The early endotoxemia PIS seamed probable originated from gut endotoxin translocation; (3)The magnitude of bacterial translocation in both portal and systemic blood and the remote systemic organs as well were recovered at 72h PIS.