| Project/Area Number |
11671271
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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 | Keio University |
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Principal Investigator |
SHIMAZU Motohide Keio University School of Medicine, Department of surgery, assistant professor, 医学部, 講師 (70124948)
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| Co-Investigator(Kenkyū-buntansha) |
TANABE Minoru Keio University School of Medicine, Department of surgery, assistant, 医学部, 助手 (50197513)
WAKABAYASHI Go Keio University School of Medicine, Department of surgery, assistant, 医学部, 助手 (50175064)
亀井 秀策 慶應義塾大学, 医学部, 外科助手 (10286495)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | ischaemic preconditioning / ischaemia reperfusion / tumor necrosis factor / microcirculation / TNFα産生 / 肝虚血再灌流障害 |
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| Research Abstract |
Background : Brief periods of hepatic ischaemia produces immediate tolerance for subsequent prolonged ischaemia. Although the beneficial effect of this ischaemic preconditioning (IPC) is recognized, the mechanism itself remains unclear.
Method : Male Wistar rats were divided into two groups : a control group that was subjected to 30 min of ischaemia + following reperfusion, and an IPC group that was subjected to 5 min of ischaemia +5 min of reperfusion +30 min of ischaemia + following reperfusion. In both groups, hepatic enzymes, histological examinations, microfluorographs, tumor necrosis factor alpha (TNFα) protein production (serum and liver tissue) and mRNA expression for TNFα within the liver tissue were analyzed during the course of reperfusion.
Results : In the IPC group, I/R injury represented by the elevation or hepatic enzymes, histological degeneration of hepatocytes, and the increase in the number of non-viable cells was markedly reduced. Moreover, endothelial-adherent leukocytes, TNFα protein production and mRNA production were also suppressed in the IPC group.
Conclusion : The mechanism underlying the protective effect of IPC in hepatic I/R injury may involve down-regulation of TNFα production and subsequent attenuation of microcircilatory injury.
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