| Project/Area Number |
07807112
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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 |
General surgery
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
MARUBAYASHI Seiji Hiroshima Univ.Medical Hospital Research Associate, 医学部・附属病院, 講師 (80144814)
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| Co-Investigator(Kenkyū-buntansha) |
SUGINO Keizyo Hiroshima Univ.School of Medicine Research Associate, 医学部, 講師 (80162882)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | hepatic ischemia-reperfusion / endotoxin / adhesion molecules / cellular injury / neutcophile / kupffer cell / 肝虚血-再灌流障害 / 肝虚血-再灌流 / 白血球 / クッパー細胞 |
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| Research Abstract |
We investigated the efficacy of the monoclonal antibodies (mAb) to adhesion molecules and the modulation of Kupffer cell function on hepatic ischemia-reperfusion injury, liver preservation and endotoxin shock induced hepatic injury. Although ischemia of the liver for 90 min did not permit survival of the animals, pretreatment with mAb to ICAM-1 and LFA-1 increased the survival rate to 57%. The number of neutrophils in the liver increased continuously up to 24 hours after reperfusion following 90 min ischemia. Pretreatment with mAb suppressed the infiltration of neutrophils and the elevation of lipid peroxide, and enhanced the recovery of hepatic ATP after reperfusion. A similar protective results we also observed in the model experiment of endotoxin shock induced liver injury. In the experiment of rat liver transplantation, a new rinse solution containing nafamostat mesilate and Kupffer cell blockade exert synergistic effects, leading to increased survival after cold-preserved liver transplantation. These results suggest that Kupffer cell and neutrophils contribute to ischemia-reperfusion injury in the liver and endotoxin shocked induced liver injury, and the pretreatment with mAb to adhesion molecules are useful for prevention of ischemic liver cell injury and endotoxin shocked liver cell injury.
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