Activation of Trypsinogen in Experimental Models of Acute Pancreatitis in Rats

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Abstract
Trypsinogen activation peptide (TAP) concentration and α2-macroglobulin-trypsin complex (α2M-T) activity were measured in two experimental models of acute pancreatitis in rats to evaluate the significance of activation of trypsinogen in acute pancreatitis. TAP concentration and α2M-T activity in serum rose significantly in trypsin-taurocholate-induced hemorrhagic acute pancreatitis, while in cerulein-induced edematous acute pancreatitis they did not rise in spite of a similar increase in immunoreactive trypsin. When rats in trypsin-taurocholate-induced pancreatitis were treated by protease inhibitor (FUT-175; nafamostat mesilate; FUT group), α2M-T activity in serum was significantly lower than that in nontreated controls (mean ± SEM, 20.8 ± 1.43 U/L in the FUT group vs 79.1 ± 24.5 in controls; p < 0.01). The survival rate at 24 h was significantly improved in the FUT group compared with the controls (70 vs 43%; p < 0.05). The increase in TAP concentration in the FUT group was similar to that in controls. The TAP concentration in pancreatic tissue at 24 h was significantly (p < 0.01) lower in the survival group (7.8 ± 0.8 ng/ml) than in the lethal group (25.9 ± 3.7 ng/ml). Activation of trypsinogen and its subsequent enzyme activity play an important role in the evolution of severe acute pancreatitis.

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