| Project/Area Number |
03304038
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Institute of Development, Aging and Cancer, Tohoku University |
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Principal Investigator |
FUJIMURA Shigehumi Institute of Development, Aging and Cncer, Tohoku University. Professor, 加齢医学研究所, 教授 (40006078)
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| Co-Investigator(Kenkyū-buntansha) |
NAMIKAWA Syoji Dpt.of Cardiovascular Surgery, Mie University, Associate Professor, 医学部, 助教授 (50024716)
KOMATSU Sakuzou Dpt.of Cardiovascular Surgery, Sapporo Medical University, Professor, 教授 (00045329)
FURUSE Akira Dpt.of Cardiovascular Surgery, Tokyo University, Professor, 医学部, 教授 (70010163)
TOMITA Masao First Dpt. of Surgery Nagasaki University, Professor, 医学部, 教授 (70039808)
KATO Harufumi Department of Surgery Tokyo Medical College, Professor, 教授 (20074768)
小柳 仁 東京女子医科大学, 教授 (90138884)
草川 實 三重大学, 医学部, 教授 (10046336)
田辺 達三 北海道大学, 医学部, 教授 (50000956)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥18,000,000 (Direct Cost: ¥18,000,000)
Fiscal Year 1993: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1992: ¥7,000,000 (Direct Cost: ¥7,000,000)
Fiscal Year 1991: ¥8,000,000 (Direct Cost: ¥8,000,000)
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| Keywords | LUNG TRANSPLANTATION / CARDIO-PULMONARY TRANSPLANTATION / PRESERVATION / DENERVATION / REJECTION / IMMUNOSUPPRESSION / PULMONARY EDEMA / 肺および心肺保存 / 保存臓器の評価 / 拒絶反応診断法 / 免疫抑制剤 / 移植後病態生理 / 移植適応基準 |
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| Research Abstract |
1.Preservation : The extracellular-type solution proved to be superior to the intracellular-type solution in pulmonary preservation, which will make a change in the basic concept of the preserbative formula. In these experints, 24-hour preserved primate lungs with Ep4 solution were demonstrated to retain equal function compared with nonpreserved lungs after transplantation.
2.Diagnosis and treatment of the acute rejection : Gradual increase in IL-2 receptor positive T cells, gradual decrease in T4/T8 ratio in theBAL and the increment of expression in mRNAs of various cytokines obtained from lung allografts were observed in the course of progressive acute rejection in the model of rat lung transplantation. TNF was demonstrated to be likely an important cytokine in the mechanisms of tissue destruction in the process of acute rejection by the tolerant model of rat lung transplantation. The assessment of lymphocyte markers in the pleural effusion proved to be also helpful in the diagnosis of acute rejection with the primate model of lung ransplantation. The measurement of the water content in lung allografts with IH-MRI revealed the increase in values of SI and T2 in the early stage of pulmonary rejection. The expression of ICAM-1 on pulmonary epithelial cells was shown, suggesting these cells as target cells of CTLs in the course of acute rejection. FK506 was demonstrated to be an potent immunosuppressant in lung transplantation, as well.
3.Posttransplantation pulmonary edema : Substance-P and the supersensitivity of alpha receptors in the pulmonary vascular bed was suspected to have a major role in developing edema of lung allograft, suggesting pulmonary denervation as a critical factor in posttransplantation pulmonary edema, togather with cell-mediated mechanisms such as platelet activating factor.
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