Pancreatic duct obstruction in rabbits causes digestive zymogen and lysosomal enzyme colocalization.

Abstract

The pancreatic duct of anesthetized rabbits was cannulated and, in some animals, flow of pancreatic exocrine secretions was blocked by raising the cannula to a vertical position. Blockage for 3-7 h caused a rapid and significant rise in serum amylase activity and an increase in amylase activity within the pancreas.

A plasma protease which is expressed during supramaximal stimulation causes in vitro subcellular redistribution of lysosomal enzymes in rat exocrine pancreas.

“…In addition to the model involving supramaximal secretagogue stimulation (4), lysosomal enzyme redistribution has been observed after short-term pancreatic duct obstruction (6) and after ingestion of a choline-deficient ethionine-supplemented diet (5). These observations suggested that those models might also involve elaboration of a plasma factor which could induce in vitro cathepsin B redistribution.…”

“…Subcellular fractionation was performed using differential centrifugation as described by Tartakoffand Jamieson (1 1) with minor modifica-tions which have been previously reported (6). Briefly, the supernatant described above was centrifuged (1,000 g X 15 min, 4C) to yield a "zymogen granule" pellet and a supernatant.…”

“…This conclusion was based on the results of morphological studies using immunolocalization techniques which demonstrated the presence ofdigestive zymogens as well as lysosomal hydrolases within the same organelle (1)(2)(3) and on the results of biochemical studies which used subcellu-lar fractionation techniques to demonstrate redistribution of cathepsin B and other lysosomal enzymes from the lysosomeenriched to the zymogen granule-enriched fraction (4,5). Subcellular redistribution and colocalization of cathepsin B with digestive zymogens was also noted to follow pancreatic duct obstruction (6). Because cathepsin B can activate trypsinogen (7) and trypsin can activate the other digestive zymogens, the colocalization of digestive enzyme zymogens with lysosomal hydrolases could lead to intracellular digestive enzyme activation and be an important triggering event in the development of acute pancreatitis (8).…”

Heart in acute pancreatitis: facts and fictions

“…4 The current theory of acute biliary pancreatitis is the common bile duct obstruction, which increases pancreatic duct pressure that led to trypsin activation and pancreatic auto-digestion. 5 Although pancreatic duct obstruction may play an important role in the pathogenesis of gallstone pancreatitis, it is not sufficient to cause the morphological changes of acute pancreatitis, 6 indicating that other events must occur if the changes induced by pancreatic duct obstruction lead to acute pancreatitis. ossible that pancreatic acinar hyperstimulation, in the presence of duct obstruction, triggers and exacerbates acute pancreatitis.…”

Haptoglobin, an acute phase reactant as marker for chronic pancreatitis – evidence from serum proteome analysis

“…It occurs when the enzymes that digest food are activated in the pancreas itself that leads to auto digestion of the pancreatic cells. [1,2] Pancreatitis may be acute or chronic. Acute pancreatitis occurs suddenly, causes severe pain in the abdomen and lasts for a few days and often, resolves completely with treatment.…”