| Project/Area Number |
08671432
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
NIMURA Yuji School of Medicine Nagoya University, Professor, 医学部, 教授 (80126888)
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| Co-Investigator(Kenkyū-buntansha) |
KANAI Michio School of Medicine Assistant Professor, 医学部, 助手 (50242871)
MIYACHI Masahiko School of Medicine Assistant Professor, 医学部, 助手 (80242874)
NAGINO Masato School of Medicine Associate Professor, 医学部, 講師 (20237564)
KONDO Satoshi School of Medicine Assosiate Professor, 医学部, 講師 (30215454)
KIMIYA Junichi School of Medicine Assosiate Professor, 医学部, 講師 (70194975)
上坂 克彦 名古屋大学, 医学部, 助手 (20283434)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | sepsis / hepatic failure / reticuloendothelial function / SIRS / multiple organ failure / bacterial infection / nitric oxide / NO synthetase / 出血性ショック再蘇生モデル / 大量肝切除モデル / Nitric Oxide / 肝網内系機能 / 手術侵襲 / サイトカイン / 術後肝不全 / 肝微小循環 / 出血性ショック / Kupper細胞 / インターロイキン |
|---|
| Research Abstract |
A stable hemorrhagic shock-resuscitation model of experimental animals for the basic study of severe infection (sepsis) or hepatic failure was established. The process of each organ dysfunction were studied and the hepatic reticuloendothelial function was objectively evaluated using our model. In this model, the evidence of systemic inflammatory response syndrome which is closely associated with multiple organ failure known as ultimate organ injury and terminal stage of sepsis were obtained, indicating that this shock model is useful to simulate sepsis and organ failure. especially hepatic failure. We also demonstrated that the organ injury. Especially hepatic failure, were associated with microcirculatory insufficiency and the accumulation of inflammatory cells (e.g. neutrophils). We, therefore, concluded that the blockage against these factors was likely to the important key for the treatment of the organ injury. The hepatic reticuloendothelial function is conceptually major host defense system to the bacterial infection such as E.coli infection and we partly elucidated the precise mechanisms of this immune response in the liver. Additionally, we elucidated that nitric oxide (NO). which is strong vaso-dilator regulating the organic microcirculation to protect from organ damages, is to be involved in bacterial killing in the liver. Whereas. 140 are recognized to have the effect of cellular injury. Therefore, regulation of selective NO synthetase would be expected to prevent hepatic dysfunction after major operation.
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