1988 Fiscal Year Final Research Report Summary
Endogenous Prostaglandin Metabolism and Endocrine and Exocrine Secretion in Obstructive Jaundiced Pancreas in Dogs.
| Project/Area Number |
62480280
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | Shinshu University Hospital |
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Principal Investigator |
KURODA Takai Shinshu University Hospital, 医学部附属病院, 講師 (60150314)
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| Co-Investigator(Kenkyū-buntansha) |
IWATSUKI Kazuhiko Department of Pharmacology, Shinshu University, 医学部薬理学, 助教授 (20004666)
山岸 喜代文 信州大学, 医学部附属病院, 助手
YAMAGISHI Kiyofumi Shinshu University Hospital
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| Project Period (FY) |
1987 – 1988
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| Keywords | Prostaglandin / CCK-8 / endocrine secretion / exocrine secretion / Pancreas |
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| Research Abstract |
The involvement of endogenous prostaglandins on-pancreatic endocrine and exocrine secretion was investigated, using the isolated perfused dog pancreas. Spontanous production of both PGE_2 and 6-ketoPGE_1 was recorded in the venous effluent. Prostaglandinproduction increased forllowing stimulation with both 10 x 10^<-11>and 20 x 10^<-11>mol of CCK-8, but was not affected by a 5 x 10^<-11> mol infusion. Insulin, glucagon and amylase releases were stimulated by 10 x 10^<-11> mol of CCK-8. Indomethacin pretreatment with 10 mg/kg totally abolished endogenous prostaglandins production, but failed to supperss insulin and glucagon response. On the other hand, amylase release was accelerated by indomethacin pretreatment. From above mentioned results, we concluded that endogenous prostaglandins do not appear to play a important role in pancreatic endocrine and exocrine secretion, but might have a cytoprotective effect on the pancreatic acinar cells damaged by CCK-8.
Next, endogenous pancreatic prostaglandin production in control and obstructive jaundice was investigated using isolated ferfused pancreas. Obstructive jaundice was made the ligation of common bile duct for three weeks. The production of both prostaglandins in obstructive jaundice, however, was higher than that in the control group on stimulation by 10 x 10^<-11>mol of CCK-8. On the incubation of the dispersed cells, prostaglandins production from jaundiced pancreatic cells was constantly and significantly higher than that from control pancreatic cells. Theses data show that enhanced endogenous prostaglandin in the obstructive jaundice might not depend on the rapid effect of blood components such as bilirubin but on the pancreatic cells degeneration owing to abnormal blood components such as bilirubin.
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