Experimental pancreatitis in the rat. Ductal factors in sodium taurocholate-induced acute pancreatitis.

Spreading of injected material and ductal resistance were studied in the rat pancreas after intraductal injection of Indian ink, human serum or sodium taurocholate. Indian ink filled the main pancreatic duct and small ductules revealing the lobular structure in macroscopic preparation. Escape into the interstitium was observed both in the macroscopic preparations and in histologic sections. Human IgG was demonstrated immunohistochemically in single acinar cells and around acinar cells after intraductal injection of human serum. The changes were most pronounced at 15 min and at 6 h after the injection but were almost resolved at 24 h. The intraductal pressure was registered during sodium taurocholate infusion. The pancreatic duct ruptured at the pressure of 82 mm Hg in average. It was concluded that in the ductal model of experimental acute pancreatitis the infusion causes ruptures in pancreatic ducts and the infusate escapes into the interstitium where it remains for several hours.

Experimental pancreatitis in the rat. Changes in pulmonary phospholipids during sodium taurocholate-induced acute pancreatitis.

Acute haemorrhagic pancreatitis was induced in rats by injecting aqueous solution of sodium taurocholate into the common biliopancreatic duct. Lecithin and lysolecithin were separated from pulmonary homogenate by thin layer chromatography and quantified by phosphorus determination. The ratio of lysolecithin to lecithin increased after the sodium taurocholate injection as well as after i.v. administration of porcine pancreatic phospholipase A2. It was concluded that phospholipase A2, released from pancreatic acinar cells into blood, may convert pulmonary lecithin into lysolecithin during acute pancreatitis. Destruction of pulmonary surfactant may contribute to the development of the adult respiratory distress syndrome as seen in patients suffering from severe acute pancreatitis.