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Treatment of multiple oragn dysfunction syndrom : establisment of endothelial cell targetting therapy

Research Project

Project/Area Number 11671170
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General surgery
Research InstitutionKYUSHU UNIVERSITY

Principal Investigator

MORISAKI Takashi  Graduate School of Medical Science KYUSHU UNIVERSITY assistant, 大学院・医学研究院, 助手 (90291517)

Co-Investigator(Kenkyū-buntansha) DOI Fukashi  Faculty of Medicines University Hospital, KYUSHU UNIVERSITY assistant, 医学部・附属病院, 助手 (10315062)
UCHIYAMA Akihiko  Faculty of Medicines University Hospital, KYUSHU UNIVERSITY assistant, 医学部・附属病院, 助手 (20294936)
Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,200,000 (Direct Cost: ¥2,200,000)
KeywordsMODS / endothelial cell / angiogenic factor / liver injury / bFGF / VEGF / regeneration / ミトコンドリア障害 / MODS / 血管内皮 / ミトコンドリア / アポトーシス
Research Abstract

Microcirculatory insufficiency resulting from endothelial cell injury is a main causative factor in sepsis-induced multiple organ dysfunction syndrome, which is a main cause of death in critical care unit. In this study, we sought to determine if endothelial cell growth factor therapy decrease organ injury in sepsis model. In in vitro experiments, we examined whether angiogenic factors such as basic fibroblast growth factor ad vascular endotthelial cell growth factor can Inhibit endothelial cell injury induced by reactive oxygen Intermediates or activated neutrophils. In 3-dimensional culture model, we showed that treatment with bFGF and VEGF could attenuate the decrease in tube formation of endothelial cells. We also demonstrated that anti-oxidative stress reagent such as N-acetyl cystein can Inhibit mitochondrial dysfunction In endothelial cells Induced by activated neutrophils and reactive oxygens such as hydrogen peroxide. In animal sepsis model, we examined the effects of angiogenic factors administration could attenuate the oorgan injury such as liver dysfunction. However we could not show the therapeutic effect of angiogenic factors administration on liver injury in this sepsis model. We are going to use both angiogenic factors and bone marrow cells for treatment of septic liver injury and oragn regeneration in animal model.

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] Tsukahara Y et al.: "Phospholipase A_2 mediates nitric oxide production by alveolar macrophages and acute lung injury in pancreatitis"Ann.Surg.. 229. 385-392 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsukahara Y et al.: "λNOS expression by activated neotrophils from patients with sepsis"AN2 J.Surg.. 71. 15-20 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsukahara Y, Morisaki T, Horita Y, Torisu M, Tanaka M.: "Phospholipase A2 mediates nitric oxide production by alveolar macrophages and acute lung Injury In pancreatitis."Ann.Surg.. 229. 385-392 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsukahara Y, Morisaki T, Kojima M, Uchiyama A, Tanaka M.: "iNOS expression by activated neutropjhils from patients with sepsis"ANZJ.Surg. 71. 15-20 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsukahara Y Morisaki T, et al. : "aNOS expression by activated neutrophils from patients with sepsis"ANI.J.Surg.. 71. 15-20 (2001)

    • Related Report
      2000 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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