Analysis for the mechanism of graft coronary arteriosclerosis
| Project/Area Number |
06671342
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Osaka University |
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Principal Investigator |
TANIGUCHI Kazuhiro Osaka University Medical School, Assistant Professor, 医学部, 助手 (90171842)
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| 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)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| 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)
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| Keywords | graft coronary arteriosclerosis / chronic rejection / heart transplantation / retransplantation / 冠動脈硬化 |
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| 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.
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Report
(3 results)
Research Products
(2 results)
