| Project/Area Number |
06671267
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
OHSHIO Gakuji Kyoto University, Surgery Graduate of Medicine, 医学研究科, 助手 (80131100)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Acute Pancreatitis / Calcium / Acinar Cells / CCK / Amylase / Lipase / pancreatic duct obstruction / CDE / 膵管閉塞 / 膵液 / 膵頭十二指腸切除術 / プロテインキナーゼC |
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| Research Abstract |
We investigated digestive enzyme release following a short-term pancreatic duct obstruction in rats. An in vivo experiment demonstrated that a 5-hour pancreatic duct obstruction reduced digestive enzyme releaase evoked both by endogenously released CCK due to pancreatico-biliary diversion and by exogenous administration of CCK-8. In vitro experiments also showed that pancreatic duct obstruction reduced the maximal CCX-8 evoked amylase secretion. Anylase secretion evoked by the calcium ionophore and phorbol nyristate acetate was also decreased. These data suggested that pancreatic duct obstruction probably interferes with the secretory process downsream of hormone receptor binding, intracellular C a release and protein kinase c activation. The in vitro anylase secretion analysis of the CDE pancreatitis demonstrated a poor response curve. The application of CCK-8 (10pM) evoked intracellular Ca oscillations. Periodicity and anplitude of oscillations in the CDE groups were not significantly different. These results suggest that other mechanisms subsequent to the onset of intracellular Ca release are likely to be involved in the inhibition of enzyme secretion.
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