ENZYME-RELEASE AND ACTIVATION OF KALLIKRE IN-KININ SYSTEMS IN EXPERIMENTAL PANCREATITIS - MEASUREMENTS IN PANCREATIC BLOOD, LYMPH AND PERITONEAL-EXUDATE

The clinical course of acute pancreatitis is strongly influenced by se condary cardiac, pulmonary and renal damage. The aim of the present st udy was to gather information about the compartment promoting the syst emic damage. Therefore the activity of lipase, phospholipase A and pla smaprokallikrein and the concentration of tissue kallikrein and kinino gen were measured in portal venous blood, pancreatic lymph and periton eal exudate. Anaesthetized pigs were subjected to fluid resuscitation to keep systemic haemodynamic parameters constant. The pancreas was is olated in situ. The pigs were randomly assigned to a control group (n = 9) or one of the two pancreatitis groups (n = 10 each). Pancreatitis was induced by i.a. infusion of free fatty acid (FFS) or retrograde i nfusion of 5% sodium taurocholate intraductally (NaT). In both pancrea titis groups the activity of lipase and phospholipase A increased. The most pronounced changes were seen in the peritoneal exsudate (phospho lipase A activity 40 min after induction: control 10.0 U/l, NaT 72.2 U /l). In both pancreatitis groups there was evidence for activation of the tissue kallikrein-kinin system in the form of an increase in the k allikrein concentration and a decrease in the kininogen concentration. Again the changes were most pronounced in the peritoneal exsudate (ti ssue kallikrein 40 min after induction: control 14.7 ng/ml, NaT 452 ng /ml).