A model of XXXX in @entity468 --role of @entity6328 .

@entity1 @entity788 @entity548 @entity6328 @entity117 @entity2918 @entity55382 @entity112 @entity3044 @entity23222 @entity468 @entity1068
Acute @entity788 was induced in @entity468 by perfusing activated pancreatic enzymes through their pancreatic ducts. The ducts had been made permeable to large molecules by one of two techniques. The @entity468 either received @entity1068 (2 ml/kg every 8 h) and @entity117 (25 mg/kg every 8 h) orally for 48 h or had their pancreatic ducts perfused for 1 h with 7.5 mM @entity23222 . When the same procedure was followed, but using @entity6328 (dmPGE2) (2 micrograms/kg X h infused intravenously for 1 h before and during ductal perfusion with activated enzymes), @entity548 developed instead. To investigate whether an increase in pancreatic blood flow or microvascular permeability (both caused by dmPGE2) was important in this phenomenon, we tested the effects of @entity3044 (which increased blood flow) and @entity112 (which increased microvascular permeability) in the model. Thus in similar experiments, either @entity3044 (0.3 micrograms/kg . min) or @entity55382 (2 micrograms/kg . min) was infused instead of dmPGE2. The animals that received @entity112 also developed @entity548 . Those that received @entity3044 did not. These observations suggested that an increase in microvascular permeability in the pancreas converted @entity788 to @entity548 . These findings suggest also that clinical studies using @entity2918 to treat @entity1 with @entity788 should be approached with caution.
