| Abstrakt: |
The purpose of the study was to compare the morphological alterations of the liver in two models of acute pancreatitis: caerulein-induced (edematous) and taurocholate-induced (necro haemorrhagic one). The experiments were performed on 24 male, Wistar rats, weighing 240-260 g. In group I (n = 8) the supramaximal stimulation with i.v. caerulein (5 micrograms/kg/h) during 12 h was applied (C-AP). Control animals (group II, n = 4) received i.v. saline (C-C). In group III (n = 8) 5% sodium taurocholate (0.2 ml/min) was injected into the bile-pancreatic duct during sterile laparotomy (T-AP). In group IV (n = 4) animals were sham operated (T-C). The specimens of the liver were excised after decapitation of rats at 12 h after beginning of caerulein infusion or intraductal injection of sodium taurocholate. The light and electron microscopy was performed. The marked hepatic lesion were found in both variants of experimental pancreatitis, however they were far more advanced in taurocholate pancreatitis. In light microscopy the dispersed foci of colliquative necrosis, degeneration of hepatocytes, swelling of Kupffer cells predominated in taurocholate pancreatitis. The glycogen deposits were depleted but lipid droplets were increased in size and number. The swelling of mitochondria, degeneration of their matrix and cristae, increase of autophagocytosis and numerous lysosomes, the lesions of sinusoids with increased activity of phagocytic cells were more evident in taurocholate pancreatitis--(more severe model of the disease). These findings document severe injury to the liver in acute pancreatitis depending on the severity of inflammatory process in pancreas. They also suggest that the liver could be not only passive target of pancreatogenic noxa in acute pancreatitis, but it could be also a defensive barrier against spreading of injuring agents on other system. This role seems to be especially evident in more severe form--taurocholate induced pancreatitis. |
