Introduction: End-to-side portacaval shunt (PCS) performed in rats is an appropriate experimental model of chronic liver insufficiency. Functional hepatic injury followed by numerous metabolic and endocrine disorders develops, as well. Due to impaired functional hepatic activity in PCS and to the well known role of the liver in CCK metabolism and elimination, delayed CCK bloodstream elimination may be responsible for increased CCK-A receptor activity. Therefore, we investigated immunohistochemical and morphometric features of duodenal CCK-cells in rats with PCS.
Material and methods: Male Wistar rats (180 - 250g body weight) were used in this experiment. The animals were divided into two groups: PCS-animals (experimental group (n=27) which underwent an operation) and C - unoperated animals [control group (n=11)].
Surgical technique: End-to-side portacaval anastomosis was created using the technique of Lee and Fisher, modified by Bismuth et al. Eight weeks, after the operation, animals were sacrificed. Pancreatic and hepatic weights were measured and samples taken from appropriate segments of the small intestine were used for morphometric and immunohistochemical CCK-cells determination. IMMUNOHISTOCHEMICAL TECHNIQUE: Peroxidase-antiperoxidase (PAP) technique described by Stenberger was applied for detection of intestinal CCK-immunoreactive cells.
Results: Our results indicate that eight weeks after operation liver weight was reduced in animals with PCS compared to control animals (p<0.01). To the contrary, in comparasion with control animals, the pancreatic wight was increased (p<0.01). In the exocrine pancreas of rats with PCS there were lipid droplets and hypertrophy of the acinus cells. The morphometric analysis of CCK-immunoreactive cells in different small intestine segments indicates that in the duodenum of animals with PCS there was a significant cell increase compared to control, unoperated animals.
Conclusion: In liver cirrhosis, plasma CCK-8 concentration increases. In PCS, performed in rats, as an experimental model of chronic liver insufficiency, proliferation of CCK-cells in the small intestine leads to pancreatic hypertrophy and hyperplasia.