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Gene therapy for acute lung injury

Research Project

Project/Area Number 08671508
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Thoracic surgery
Research InstitutionAkita University

Principal Investigator

IZUMI Keiichi  Akita University School of Medicine Assistant Professor, 医学部, 講師 (60176237)

Co-Investigator(Kenkyū-buntansha) MINAMIYA Yoshihiro  Akita University School of Medicine Assistant Professor, 医学部, 講師 (30239321)
KITAMURA Michihiko  Akita University School of Medicine Associate Professor, 医学部, 助教授 (10153131)
Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1996: ¥1,800,000 (Direct Cost: ¥1,800,000)
Keywordsneutrophil / endothelial cell / transendothelial migration / 肺移植 / 白血球 / 活性酸素 / 急性肺障害 / 接着分子
Research Abstract

It has been reported that reperfusion is the most important factor in ischemia-reperfusion injury. However, causes of ischemia-reperfusion injury in the lung are controversial, because oxygen is always supplied if ventilation continues. Therefore, we hypothesized that nonhypoxic ischemia without reperfusion is sufficient for lung injury. To test our hypothesis, we measured both hydrogen peroxide (H_2O_2)production in the pulmonary circulation by digital imaging fluorescent dichlorofluorescein and the microvascular permeability (MVP) by the Evans blue extravasation technique in the nonhypoxic ischemia rat lung. We made a nonhypoxic ischemia rat lung by clamping the left pulmonary artery. Both H_2O_2 production and MVP increased in the nonhypoxic ischemia rat lung. We also determined the effect of oxygen removal by clamping bronchus in advance of pulmonary artery occlusion, intercellular adhesion molecule-1 (ICAM-1) neutralization with monoclonal antibody 1A29, and plateletactivating factor (PAF) receptor antagonist CV6209 on H_2O_2 production and MVP.These treatmrnts inhibited both H_2O_2 production and MVP increase. At high power viewing of the fluorescent dichlorofluorescein image, H_2O_2 was detected in the leukocytes within pulmonary capillaries. These data indicate that the nonhypoxic ischemia without reperfusion alone causes radical production and increases MVP.Furthermore, PAF and ICAM-1 contribute to these reactions.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] Yoshiro Minamida et al.: "Platelet-activating faction mediates intercallular adhosion molecule-1-deperclent rawcall production in the morbypoxic rat lurg" American Journal of Respiretory cell and Moleculer Biology. (印刷中).

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] 1) Yoshihiro Minamiya et al.: "Platelet-activating factor mediates intercellular adhesion molecule-1-dependent radical production in the nonhypoxic ischemia rat lung." Am.J.Respir.Cell Mol.Biol.(inpress).

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Yoshihiro Minamiya: "Platelet-activating factor mediates intercellular adhesion molecule-1-depen-dent radical production in the nonhypoxic ischemia rat lung" American Journal of Respiratory Cell and Molecular Biology. (in press).

    • Related Report
      1997 Annual Research Report

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Published: 1996-04-01   Modified: 2017-10-11  

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