The data suggest that an increase in capillary permeability may be an important step in the pathogenesis of acute pancreatitis. Albumin, dextran 70, and dextran 40 effectively reduced the FFA-induced injury response in this model, but dextran 20 was of no benefit. This suggests that the change in capillary permeability results from an increase in capillary pore size sufficient to allow the escape of molecules with molecular weights of 20,000 but not those substances whose molecular weights are greater than 40,000. The role that enzyme extravasation plays in the pathogenesis of acute pancreatitis in this experimental model or in other experimental or clinical situations remains unclear. It is possible that the capillary injury that occurs early in the pathogenesis of pancreatitis is mediated through enzyme release. However, the failure of aprotinin (Trasylol), an enzyme inhibitor, to modify pancreatitis clinically or experimentally, as previously demonstrated in this model, suggests that in edematous pancreatitis autodigestion may not play an important role.
|Original language||English (US)|
|Number of pages||7|
|State||Published - Dec 1 1984|
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