Early changes in pancreatic acinar cell XXXX signaling after @entity788 .

@entity1 @entity788 @entity2426 @entity35 @entity13216 @entity19 @entity4 @entity5990 @entity8586 @entity460 @entity141 @entity11008 @entity491 @entity12828 @entity934
Intracellular @entity141 -changes not only participate in important signaling pathways but have also been implicated in a number of disease states including acute @entity788 . To investigate the underlying mechanisms in an experimental model mimicking @entity1 @entity5990 -induced @entity788 , we ligated the pancreatic duct of @entity35 and NMRI @entity19 for up to 6 h and studied intrapancreatic changes including the dynamics of [ @entity141 ](i) in isolated acini. In contrast to bile duct ligation, @entity788 induced intra-pancreatic trypsinogen activation, @entity491 , @entity12828 , and pancreatic @entity4 and increased lung myeloperoxidase activity. Although resting [ @entity141 ](i) in isolated acini rose by 45% to 205 +/- 7 nmol, the @entity934 - and @entity8586 ( @entity13216 )-stimulated @entity460 peaks as well as the amylase secretion declined, but neither the [ @entity141 ](i)-signaling pattern nor the amylase output in response to the @entity141 -ATPase inhibitor @entity2426 nor the secretin-stimulated amylase release were impaired by pancreatic duct ligation. On the single cell level pancreatic duct ligation reduced the percentage of cells in which submaximal secretagogue stimulation was followed by a physiological response (i.e. @entity141 oscillations) and increased the percentage of cells with a pathological response (i.e. peak plateau or absent @entity141 signal). Moreover, it reduced the frequency and amplitude of @entity141 oscillation as well as the capacitative @entity141 influx in response to secretagogue stimulation. Serum pancreatic enzyme elevation as well as trypsinogen activation was significantly reduced by pretreatment of animals with the @entity460 chelator @entity11008 . These experiments suggest that @entity788 rapidly changes the physiological response of the exocrine pancreas to a @entity141 -signaling pattern that has been associated with premature digestive enzyme activation and the onset of @entity788 , both of which can be prevented by administration of an intracellular @entity460 chelator.
