| Project/Area Number |
06671292
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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 | Oita Medical University |
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Principal Investigator |
YOSHIDA Takanori Oita Medical University, Dept.of Surg I,Assistant Professor, 医学部・講師(学内) (90220649)
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| Co-Investigator(Kenkyū-buntansha) |
KITANO Seigo Oita Medical University, Dept.of Surg I,Associate Professor, 医学部, 助教授 (90169871)
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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 |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | portal hypertension / hyperdynamic state / glucagon |
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| Research Abstract |
The role of glucagon as a mediator of gastric hyperdynamic circulation, induced by carbon tetrachloride (CCl_4), was assessed in cirrhotic rats. A selective elimination of pancreatic glucagon from the circulation was achieved by the intravenous infusion of a glucagon antiserum. Gastric blood flow was measured by laser-Doppler flowmetry. The glucagon antiserum had no effect on the blood flow in the stomach in control rats, while in cirrhotic portal hypertensive rats, the glucagon antiserum significantly reduced gastric blood flow (30%). The glucagon antiserum did not completely exclude the gastric hyperdynamic state in the cirrhotic rats. It would thus appear that glucagon contributes to a portion of the gastric hyperdynamic circulation associated with cirrhotic portal hypertension.
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