| Project/Area Number |
02670600
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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 | Chiba University |
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Principal Investigator |
BABA Masayuki Chiba University, Research Instructor, 医学部, 助手 (00143305)
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| Co-Investigator(Kenkyū-buntansha) |
SAITOH Yukio Chiba University, Resident, 医学部, 医員
URABE Norikazu Chiba University, Assistant Professor, 医学部, 講師
SHIBA Mitutoshi Chiba University, Research Instructor, 医学部, 助手 (20162620)
FUJISAWA Takehiko Chiba University, Associate Professor, 医学部, 助教授 (80110328)
YAMAGUCHI Yutaka Chiba University, Professor, 医学部, 教授 (80009448)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Lung transplantation / Prostaglandin I2 / Rejection / Lung preservation / Cytotoxic activity / Endothelial derived relaxing factor / Cyclic GMP / 血管内皮細胞 / EDRF / cGMP / プリスタグランジンI_2 |
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| Research Abstract |
Histological changes of the grafted lungs during acute lung allograft rejection To investigate the relation between the injury to endothelial cells and specific immunoresponse during lung allograft rejection, we studied for donor specific cytotoxic activity in recipient PBL and histological changes of the grafted lung. It was found that there was exudation, which appeared to be caused by hyperpermiability of endothelial cells, in the alveolar space at the time of increased cytotoxic activity. It is considered that an evaluation of viability in endothelial cells is essential to study for lung injury due to rejection.
Changes of Prostaglandin I2 release capacity from dog lungs PGI2 releasing capacity induced by bradykinin from endothelial cells of dog lung which were injured by normothermic preservation, and correlation between the changes in vitro and gas exchanie function of grafted lung in vivo was investigated. It was found that PGI2 releasing capacity in injured lungs showed significant decrease. It is considered that this assay is useful to estimate the viability of endothelial cells.
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