Objective: To investigate pancreatic ischemia and abnormal metabolism of eicosanoids in acutehaemorrhagic necrotizing pancreatitis (AHNP) and the effects of emodin or sandostatin on them. Methods: Inrats with AHNP triggered with sodium taurocholate, the pancreatic blood flow (PBF) was detected with computerized tissue blood flowmeter, and plasma thromboxane B2 (TXB2), 6-keto-prostaglandin Fla.(6-keto-PGFla)and prostaglandin E2 (PGE2) were determined with radioimmunoassay. Results: There was a significant decrease of PBF in the early stage of AHNP. Compared with that in the non-treated group, significant improvement of PBF was demonstrated in emodin as well as in sandostatin group which showed reduced PBF followinginfusion of sandostatin before AHNP was triggered. In the non-treated group, plasma TXBZ was significantlyhigher, with an increase of 4. 5 times, than that in sham--operated group, while 6-keto-PGFla and PGE2 tendedto decrease. The above mentioned abnormal metabolism of eicosanoids was blocked either in emodin or in sandostatin group in which lessened damage of acinar cells was shown by pathologic scoring or transmission electronmicroscope. Both groups shared significantly lower mortalities than the non-treated group. Conclusions: Eitheremodion or sandostatin could partly reverse the decrease of PBF in the early stage of AHNP, which may be ascribed at least in part to inhibition of abnormal metabolism of eicosanoids and improvement of pancreatic cytoprotection, and combined application of the two drugs is likely to have synergetic action. Objective: To investigate pancreatic ischemia and abnormal metabolism of eicosanoids in acutehaemorrhagic necrotizing pancreatitis (AHNP) and the effects of emodin or sandostatin on them. Methods: Inrats with AHNP triggered with sodium taurocholate, the pancreatic blood flow (PBF) was detected with computerized tissue Blood flowmeter, and plasma thromboxane B2 (TXB2), 6-keto-prostaglandin Fla. (6-keto-PGFla) and prostaglandin E2 (PGE2) were determined with radioimmunoassay. Results: There was a significant decrease of PBF in the early stage of Compared with that in the non-treated group, significant improvement of PBF was demonstrated in emodin as well as in sandostatin group which showed reduced PBF following infusion of sandostatin before AHNP was triggered. In the non-treated group, plasma improvement in PBF was significantlyhigher, with an increase of 4. 5 times, than that in sham-operated group, while 6-keto-PGFla and PGE2 tended to decrease. The above mentioned abnormal metabolism of eicosa noids was blocked either in emodin or in sandostatin group in which lessened damage of acinar cells was shown by pathologic scoring or transmission electronmicroscope. Both groups shared significantly lower mortalities than the non-treated group. Conclusions: Eitheremodion or sandostatin could partly reverse the decrease of PBF in the early stage of AHNP, which may be ascribed at least in part to inhibition of abnormal metabolism of eicosanoids and improvement of pancreatic cytoprotection, and combined application of the two drugs is likely to have synergetic action.