WHATEVER the precipitating cause may be, enzymatic digestion of the pancreatic tissue by proteolytic enzymes is probably a factor in the pathogenesis of acute pancreatitis. The vascular collapse which sometimes occurs with acute pancreatitis may be attributable in part to vasoactive substances of the blood, activated by trypsin or kallikrein which enter the blood from the damaged pancreas.1 Therefore "the aim of the treatment of acute pancreatitis," according to Forell,2 "is to keep the enzyme content of the gland as low as possible, to inactivate the already active trypsin and kallikrein in the pancreas and blood, and finally to stop the intrapancreatic trypsin activation."
Several protease inhibitors, especially inhibitors of trypsin such as soybean inhibitors, Ovomucoid,3-6 benzethonium chloride, and even serum albumin8 have been used in efforts to modify the course of experimental pancreatitis but with limited or no success. Beneficial effects of a kallikrein and
SINGH LM, HOWARD JM. Studies of TrasylolEvaluation of Trasylol Against the Hypotensive Effects of Trypsin and Kallikrein. Arch Surg. 1965;91(4):635-639. doi:10.1001/archsurg.1965.01320160089021