title: [Effects and mechanism of emodin and sandostatin on pancreatic ischemia in acute haemorrhagic necrotizing pancreatitis].
abstract: OBJECTIVE
  To investigate pancreatic ischemia and abnormal metabolism of eicosanoids in acute haemorrhagic-necrotizing pancreatits (AHNP) and the effects of emodin or sandostatin on them.
  
  
  METHODS
  Rats with AHNP were triggered with sodium taurocholate; the pancreatic blood flow (PBF) was detected with computerized tissue blood flowmeter, and plasma prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane (TXB2) were determined with radioimmunoassay.
  
  
  RESULTS
  There was a significant decrease of PBF in the early stage of AHNP. Compared with that in the untreated group, significant improvement of PBF was demonstrated in emodin as well as in sandostatin group which showed reduced PBF following infusion of sandostatin before triggering AHNP. In untreated group plasma TXB was significantly higher, with an increase of 4.5 times, than that in sham-operated group while 6-keto-PGF1 alpha or PGE2 tended to decrease. The above mentioned abnormal synthesis of eicosanoids was blocked either in emodin or in sandostatin group in which lessened damage of acini cells was shown by pathologic scoring or transmission electron microscope. Both of the two groups shared significantly lower mortalities than the untreated group.
  
  
  CONCLUSIONS
  Either emodion 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 synthesis of eicosanoids and improvement of cytoprotection of acini cells, and combined application of the two drugs might promise positively synergetic action as well.
authors.affiliation: Ruijin Hospital, Shanghai Second Medical University.
authors.forename: J X
authors.initials: JX
authors.lastname: Wu
authors.forename: J Y
authors.initials: JY
authors.lastname: Xu
authors.forename: Y Z
authors.initials: YZ
authors.lastname: Yuan
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D015232:Dinoprostone / Q000097:blood; D004642:Emodin / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D008297:Male; D015282:Octreotide / Q000031:analogs & derivatives* / Q000494:pharmacology; D010179:Pancreas / Q000098:blood supply / Q000648:ultrastructure; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood* / Q000139:chemically induced / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D013656:Taurocholic Acid; D013929:Thromboxane B2 / Q000097:blood
chemical_list: D004791:Enzyme Inhibitors; C045210:3-Tyr-octreotide; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D013656:Taurocholic Acid; D015232:Dinoprostone; D004642:Emodin; D015282:Octreotide