| Project/Area Number |
07671414
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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 | Yokohama city university |
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Principal Investigator |
KUNISAKI Chikara Second Department of Surgery, School of medicine, Yokohama city university, 医学部, 附属病院助手 (70264611)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAOKA Hiroyuki Second Department of Surgery, School of medicine, Yokohama city university, 医学部, 講師 (90230317)
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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 |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1996: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
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| Keywords | oxigen free radicals / adhesion molecules / ischemia-reperfusion injury / microcirculatory disturbance / prostaglandin E1 (PGE1) / intercellular adhesion molecule-1 (ICAM-1) / 虚血再灌流障害 / 肝 / 再灌流障害 / 類洞内皮細胞障害 / プロスタグランジンE1 |
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| Research Abstract |
The AIM of this study is to investigate the involvement of adhesion molecules and oxigen free radicals in ischemia-reperfusion injury of the liver. RESULTS: [Exam 1] 1) ALT and AST were significantly decreased by PGE1 or anti ICAM-1 administration. PGE1 increased the bile production significantly. They were also decreased in neutrophil depleted rats. 2) IL-8 was not influenced by administration of PGE1 nor anti-ICAM-1 antibody. 3) The retention rate of fluorescence labeled hyaluronic acid was significantly decreased by PGE1, anti-ICAM-1 administration or in neutrophil depleted rats. [Exam 2] After reperfusion adherent leukocytes had progressively increased significantly in Control group but not in PGE1 and anti-ICAM-1 group. [Exam 3] The expression of LFA-1 and Mac-1 by flow cytometric study was not affected by PGE1. However ICAM-1 on endothelium was suppressed by PGE1 administration. [Exam 4] Oxygen free radicals derived from hepatocytes and endothelium were decreased by PGE1 administration. CONCLUSION: These data indicate that adhesion molecules plays a pivotal role in liver injury after reperfusion. Neutrophil adhesion to endothelial cells caused microcirculatory disturbance after ischemia- reperfusion. PGE1 protects against liver injury through the reduction of neutrophil-endothelial cell adhesion by supression of ICAM-1 expression.
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