AIM: To explore the relationship between gastric and intestinal microcirculatory impairment and inflammatory mediators released in rats with acute necrotizing pancreatitis (ANP). METHODS: A total of 64 rats were randomized into control group and ANP group. ANP model was induced by injection of 5% sodium taurocholate under the pancreatic membrane. Radioactive biomicrosphere technique was used to measure the gastric and intestinal tissue blood flow at 2 and 12 h after the induction of ANP, meanwhile serum phospholipase A2 (PLA2) activities and interleukin-1β levels were determined. Pathologic changes in pancreas, gastric and intestinal mucosae were studied. RESULTS: The gastric blood flow in ANP group (0.62±0.06 and 0.35±0.05) mL/(min·g) was significantly lower than that in control group (0.86±0.11 and 0.85±0.06) mL/(min·g) (P<0.01) at 2 and 12 h after induction of ANP. The intestinal blood flow in ANP group (0.80±0.07 and 0.50±0.06) mlV(min·g) was significantly lower than that in control group (1.56±0.18 and 1.61±0.11) mL/(min·g) (P<0.01). Serum PLA2 activities (94.29±9.96 and 103.71± 14.40) U/L and IL-1β levels (0.78±0.13 and 0.83±0.20)μg/L in ANP group were higher than those in control group (65.27±10.52 and 66.63±9.81) U/L, (0.32±0.06 and 0.33±0.07)μg/L (P<0.01). At 2 and 12 h after introduction of the model, typical pathologic changes were found in ANP. Compared with control group, the gastric and intestinal mucosal pathologic changes were aggravated significantly (P<0.01) at 12 h after induction of ANP. Gastric and intestinal mucosal necrosis, multiple ulcer and hemorrhage occurred. CONCLUSION: Decrease of gastric and intestinal blood flow and increase of inflammatory mediators occur simultaneously early in ANP, both of them are important pathogenic factors for gastric and intestinal mucosal injury in ANP. AIM: To explore the relationship between gastric and intestinal microcirculatory impairment and inflammatory mediators released in rats with acute necrotizing pancreatitis (ANP). METHODS: A total of 64 rats were randomized into control group and ANP group. ANP model was induced by injection of 5 % sodium taurocholate under the pancreatic membrane. Radioactive biomicrosphere technique was used to measure the gastric and intestinal tissue blood flow at 2 and 12 h after the induction of ANP, meanwhile serum phospholipase A2 (PLA2) activities and interleukin-1 β levels were determined. Pathologic RESULTS: The gastric blood flow in ANP group (0.62 ± 0.06 and 0.35 ± 0.05) mL / (min · g) was significantly lower than that in control group (0.86 ± 0.11 and 0.85 ± 0.06) mL / (min · g) (P <0.01) at 2 and 12 h after induction of ANP. The intestinal blood flow in ANP group (0.80 ± 0.07 and 0.50 ± 0.06) mlV (min · g) was significantly lower than that Serum PLA2 activities (94.29 ± 9.96 and 103.71 ± 14.40) U / L and IL-1β levels (0.78 ± 0.13 and 1.61 ± 0.11) mL / (min · g) 0.83 ± 0.20) μg / L in ANP group were higher than those in control group (65.27 ± 10.52 and 66.63 ± 9.81) U / L, (0.32 ± 0.06 and 0.33 ± 0.07) μg / L, respectively compared with control group, the gastric and intestinal mucosal pathologic changes were aggravated significantly (P <0.01) at 12 h after induction of ANP. Gastric and intestinal mucosal necrosis , multiple ulcer and hemorrhage occurred. CONCLUSION: Decrease of gastric and intestinal blood flow and increase of inflammatory mediators occur early in ANP, both of them are important pathogenic factors for gastric and intestinal mucosal injury in ANP.