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Alteration of Kupffer Cell Function in Hepatic Ischemia and Reperfusion Injury

Research Project

Project/Area Number 07671377
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Digestive surgery
Research InstitutionHamamatsu University School of Medicine

Principal Investigator

SUZUKI Shohachi  Hamamatsu University of Medicine, The Second Department of Surgery, Assistant Professor, 医学部附属病院, 助手 (20196827)

Co-Investigator(Kenkyū-buntansha) NAKAMURA Satoshi  Hamamatsu University School of Medicine, The Second Department of Surgery, Assis, 医学部, 助教授 (00090027)
Project Period (FY) 1995 – 1996
Project Status Completed (Fiscal Year 1996)
Budget Amount *help
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
KeywordsHepatic ischemia / Reperfusion Injury / Kupffer cell / Tumor necrosis factor-alpha / Gadolinium chloride / 肝 / 虚血
Research Abstract

The present study was designed to determine whether the duration of hepatic ischemia with or without blockade of Kupffer cell function affects reticuloendothelial phagocytic activity and tumor necrosis factor (TNF) -alpha production in the early phase of reperfusion, and to clarify the welltolerated ischemic period for the liver. Male rats were pretreated with either normal saline (NS group) or gadolinium chloride (7 mg/kg) for 2 days to inhibit Kupffer cell function (GC group) and were subjected to 30,60, or 90 minutes of total hepatic ischemia. The animals tolerated well for 30 and 60 minutes of hepatic ischemia in both groups. Although the 7-day survival rate of the NS group decreased to 28% after 90 minutes of hepatic ischemia, that of the GC group significantly improved to 68% (p<0.01). In the NS group, the plasma alanine transaminase (ALT) and TNF-alpha levels after reperfusion increased with the length of hepatic ischemia. Extremely high TNF-alpha levels (142.5(]SY.+-。[)82.4 pg/ … More ml) and ALT levels (7,892(]SY.+-。[)1,817 IU/L) were observed at 1 and 6 hours after reperfusion following 90 minutes of hepatic ischemia. In the NS group, the phagocytic index (PI) after 60 minutes of reperfusion following 90 minutes of hepatic ischemia showed significant depression compared to the preischemic level and the value after 30 or 60 minutes of ischemia. The GC group had significantly lower plasma ALT and TNF-alpha levels as well as significantly less polymorphonuclear leukocyte infiltration in the liver compared to the NS group. The preischemic PI was significantly inhibited in the GC group when compared with that in the NS group, but PI in the GC group did not change significantly after reperfusion, irrespective of the ischemic time. This study demonstrated that warm ischemia of up to 60 minutes is tolerable for normal rat liver without a detrimental effect on phagocytic activity, whereas 90 minutes of hepatic ischemia causes a decrease of PI,increased TNF-alpha production, and a high mortality after reperfusion. Modulation of Kupffer cell function may have the potential to prevent reperfusion injury after hepatic ischemia, which may allow safe prolongation of the ischmic time Less

Report

(3 results)
  • 1996 Annual Research Report   Final Research Report Summary
  • 1995 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Serizawa A: "Involvement of platelet-activating factor in cytokine production and neutrophil activation after hepatic ischemia-reperfusion." Hepatology. 23. 1656-1663 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Suzuki S: "Role of Kupffer cells and the spleen in modulation of endotoxin-induced liver injury after partial hepatectomy." Hepatology. 24. 219-225 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Serizawa A,Nakamura S,Suzuki S,Baba S,Nakano M: "Involvement of platelet-activating factor in cytokine production and neutrophil activation after hepatic ischemia-reperfusion." Hepatology. 23. 1656-1663 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Suzuki S,Nakamura S,Serizawa A,Sakaguchi T,Konno H,Mura H,Kosugi I,Baba S: "Role of Kupffer cells and the spleen in modulation of endotoxin-induced liver injury after partial hepatectomy." Hepatology. 24. 219-225 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Serizawa A: "Involvement of platelet-activating factor in cytokine production and neutrophil activation after hepatic ischemia-reperfusion." Hepatology. 23・6. 1656-1663 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] Suzuki S: "Role of Kupffer cells and the spleen in modulation of endotoxin-induced liver injury after partial hepatectomy." Hepatology. 24・1. 219-225 (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1995-04-01   Modified: 2016-04-21  

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