| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
In order to elucidate the pathophysiology in the development of alcoholic chronic pancreatitis, we examined the effects of acute and chronic intragastric ethanol administration on the motility of papillary sphincter zone and pancreatic ductal pressure, using Japanese monkeys.
1) Manometry of papillary sphincter zone and pancreatic ductal pressure : A duodenofiberscope ( Olympus JF-1T ) was inserted in the duodenum through the gatric fistula,formerly made operatively. Pressures were recorded with the 4 Fr. microtransducer,inserted in the sphincter of Oddi and main pancreatic duct. The results were as follows : Peak and basal pressures were decreased during 10-20 minutes and contraction frequency was increased during 15-35 minutes after intragastric ethanol(10 ml of 30%) injection, but no change was recorded in the pancreatic ductal pressure in the first 20 minutes.
2) Chronic ethanol administration : After ethanol (1.0% of averaged 800 ml/day) feeding for 6 months ad libitum, peak and basal pressures were decreased and contraction frequency was elevated, and pancreatic ductal pressure was elevated; significantly.
3) Histological findings of the pancreas in chronic alcohol-fed monkeys : In light microscopy, acinar cells degeneration and inflammatory cells infiltration were not observed. But in electron microscopy, dilatation of cisterna of rough endoplasmic reticulum in acinar cells and fibroblasts, and accumulation of collagen fibers in the interstitial space were observed.
In conclusion , acute ethanol administration affected on papillary function, and chronic administration affected on the motility of papillary sphincter zone and pancreatic ductal pressure as well as on the protein synthesis of acinar cells ( exocrine hypersecretion ) in Japanese monkeys. It may lead us to the hypothesis that papillary dysfunction , elevated pancreatic ductal pressure and exocrine hypersecretion may play roles in the pathogenesis of human alcoholic chronic pancreatitis.
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