Kakizaki G, Sasahara M, Aikawa T, Matsuo M, Sugawara Y, Nakamura K, Endo S, Ito Y
Shizugawa Hospital, Japan.
Int J Pancreatol. 1987 Apr;2(2):101-16. doi: 10.1007/BF03015003.
To elucidate the pathogenesis of chronic alcoholic pancreatitis, light-microscopic and electron microscopic observations of pancreases from Wistar strain rats given 20% ethanol ad lib, instead of water, were performed. Results were as follows: (1) In 3 (11%) rats, focal lobular unit acinar cell damage was observed under light-microscopy. In these cases, the intercalated ducts and centroacinar cells showed proliferation independently of protein plugs in ducts. (2) After ethanol intake, several degenerative changes in the acinar cells and ductular cells were observed under electron microscopy. The earliest and most consistent change was the irregular formation of microvilli and interdigitation between the parenchymal cells, accompanied by widening of the intercellular space, especially between the acinar and centroacinar cells. After three months of ethanol intake, an increase in the lysosomes and mitochondrial alteration occurred in acinar cells, and after six months of ethanol ingestion, there was tortuous ductular proliferation accompanied by the degeneration of the ductular cells. In addition to these parenchymal changes, the capillary endothelium and nervous tissue of the pancreas showed occasional degenerative changes after three to six months of ethanol intake. These results suggest that repeated degeneration and regeneration of the ductular cells results in deformation of ductular structures, with subsequent stenosis, and represents the primary event in the development of chronic alcoholic pancreatitis in rats.
