Abstract
To study the importance of a disturbed energy metabolism for the development of acute pancreatitis (AP) rats pretreated either by induction of a juice edema or by intraductal trypsin instillation were subjected to temporary pancreatic ischemia. By means of a scoring system quality and quantity of pathomorphologic parameters were quantified 24 h postoperatively. There was a clear correlation between macroscopic and histologic scores independent of the model used. While a juice edema or 40 min ischemia alone did not induce AP, a combination of both led in half of the animals treated to AP. This was mainly characterized by extrapancreatic fat necrosis. Besides less specific fat necrosis the histologic examination of the pancreas revealed acinar necroses at the periphery of the lobules as a frequent injury pattern. After trypsin injection a persistent pancreatic edema, hemorrhages, fat and parenchymal necroses were typical findings. Both focal centro-lobular and extended sublobular or lobular necroses were histologically observed. An additional temporary ischemia augmented significantly the severity of findings, however, their quality was not essentially changed. From the present results it can be concluded that an alteration of the pancreatic energy metabolism, e.g. by hypoperfusion or ischemia, may be an important pathogenic factor in precipitating experimental AP.
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