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Analysis for the mechanism of graft coronary arteriosclerosis

Research Project

Project/Area Number 06671342
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Thoracic surgery
Research InstitutionOsaka University

Principal Investigator

TANIGUCHI Kazuhiro  Osaka University Medical School, Assistant Professor, 医学部, 助手 (90171842)

Co-Investigator(Kenkyū-buntansha) SAWA Yoshiki  Osaka University Medical School, Assistant Professor, 医学部, 助手 (00243220)
NAKATA Seizoh  Osaka University Medical School, Assistant Professor, 医学部, 助手 (50116068)
SHIRAKURA Ryota  Osaka University Medical School, Professor, 医学部, 教授 (00116047)
Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,500,000 (Direct Cost: ¥1,500,000)
Keywordsgraft coronary arteriosclerosis / chronic rejection / heart transplantation / retransplantation / 冠動脈硬化
Research Abstract

We developed long-term acceptance of rat heart allografts induced by short-course treatment of FK506 in both MHC antigen mismatch and non-MHC,minor antigen mismatch combinations. Graft coronary arteriosclerosis (GCAS) was occurred in these long surviving grafts Definite GCAS change was clarified on day 40 after transplantation. In spite of FK506 treatment, in vitro cellular activities analyzed recipient spleen T cells were recognized in early phase of posttransplantation in both MHC and non-MHC mismatch combinations. Anti-donor antibodies were detected in some cases of MHC mismatch combination, but not in any cases of non-MHC mismatch combination throughout the observation time. These data suggest that anti-donor antibody is not essential for GCAS induction. We examined that whether continuous allostimulation was necessary for GCAS induction by retransplantation of allografts back into the original donor strain in this established GCAS model. We call this technique return transplantation. To ascertain the point at which the GCAS changes become irreversible, the grafted hearts were removed on day 3,5,7, or 9, and retransplanted into the donor strain rats to prevent further immunological stimulation. These retransplanted grafts were examined to evaluate the grade of GCAS on day 40. Retransplanted heart allografts back into the original donor strain did not prevent GCAS if the graft had resided in the first recipient for up to 5 days after first transplantation. In conclusion, return transplantation technique revealed that graft coronary arteriosclerosis was induced between 3 and 5 days posttransplantation and develop without subsequent allostimulation.

Report

(3 results)
  • 1995 Annual Research Report   Final Research Report Summary
  • 1994 Annual Research Report
  • Research Products

    (2 results)

All Other

All Publications (2 results)

  • [Publications] H. izutani, S. Miyagawa, R. Shirakura, G. Matsumiya, S. Nakata, Y. Shimazaki, H. Matsuda: "Evidence that graft coronary arteriosclerosis begins in the early phase after transplantation and progresses without chronic immunoreaction" Transplantation. 60. 1073-1079 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] H.izutani,R.Shirakura,et al.: "Evidence that graft coronary arteriosclerosis begins in the early phase after transplantation and progresses without chronic immunoreaction" Transplantation. 60. 1073-1079 (1995)

    • Related Report
      1995 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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