| Project/Area Number |
06454377
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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 | AKITA UNIVERSITY |
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Principal Investigator |
KOYAMA Kenji Akita University School of Medicine Professor, 医学部, 教授 (80004638)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Tsutomu Akita University School of Medicine Assistant Surgeon, 医学部, 助手 (90235367)
FURUYA Tomoki Akita University School of Medicine Assistant Surgeon, 医学部, 助手 (60250891)
SATO Yasuhiko Akita University School of Medicine Assistant Surgeon, 医学部, 助手 (80235407)
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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 |
¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1994: ¥6,000,000 (Direct Cost: ¥6,000,000)
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| Keywords | Hepatic injury / Heat Shock Protein / DNA injury / NICK / Ischemia and reperfusion-injury / Heat Shock protein / 近赤外分光々光計 / 阻血再潅流障害 |
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| Research Abstract |
We have already revealed that the increase of oxygen content in the hepatic blood flow improved liver function. It is also reported that the heat shock protein (Hsp) in hepatocyte has close relationship to DNAinjury and its improvement depending on ATP metabolism, which suggests the induction of Hsp in hepatocytes by some suitable method can be useful for protection of the liver from operative insult.
On these bases, we made a plan to increase the safety of hepatectomy for hepatoma with cirrhosis by hepatic oxygenation and advance induction of hepatocyte Hsp using hyperthermia. Although many studies on the hepatic functional reserve have been conducted, the results were used for discrimination of the patients with potential hepatic failure after surgery, who are to be excluded from hepatectomy. Focusing on such patients, we attempted to increase the functional reserve of the liver to bear the operative insult by changing the intrinsic factors such as oxygen concentration in the hepatic blood flow or induction of intracellular Hsp.
Following results are obtained in this experiment using rats.
1). content and localisation of Hsp in the liver changed according to the extent of hepatic dysfunction.
2). Hsp73 is induced in the hepatocyte by immersion of the whole body in water of 43 degree (C), and cahnge its location between nucleus andcytoplasm.
3). Induction of Hsp in volume measured by immunobloting cahnged depending on the duratioon and time of heat exposure.
4). In the rats with advance induction of Hsp, the liver injury by hepatic ischemia, endotoxin infusion and administration of thioacetamide could be protected.
5). Hepatic venous back flow seemed to protect hepatocyte from ischemic injury by inflow occlusion.
These results can support the significance of hepatic oxygenation and advance induction of Hsp to increase the hepatic functional reserve, and clinical application can be recommended.
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