| Co-Investigator(Kenkyū-buntansha) |
SHINKAI Mahito Tokyo Women's Medical College, Dept.of Surgery, Assistant, 医学部, 助手 (10216210)
FUJITA Shougo Tokyo Women's Medical College, Dept.of Surgery, Assistant, 医学部, 助手 (58257020)
小山 一郎 東京女子医科大学, 医学部, 助手 (10266760)
船越 陽一 東京女子医科大学, 医学部, 助手 (20238653)
藤田 省吾 東京女子医科大学, 医学部, 助手 (70209055)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
Prevention of hyperacute xenograft rejection by polyclonal antibodies against donor luymphocytes and red cells.
T.Murakami, S.Hujita, Y.Hayasaka, M.Shinkai, Y.Funakoshi, T.Kawai, S.Fuchinoue, S.Teraoka, T.Agishi, and K.Ota.
Dept.of Surgery, Kidney Center, Tokyo Womens Medical College, Tokyo, Japan.
Intravenous administration of immunoglobulin (IVIG) at a high dosage has been reported to delay an initiation of hyperacute rejection (HAR) of the discordant xeno-grafts. In order to investigate possibility of preventing HAR of guinea pig hearts grafted to Lewis rats by IVIG,specific polyclonal antibodies were produced by immunizing rabbits against guinea pig lymphocytes and red cells (anti-GP-pAb)
Immediately before transplantation, the Lewis rats intravenously received either 1 ml of 20% human albumin as a control or 1.5-30mg/kg of the antibodies. Contraction time of the vascualized cardiac xenografts was extended from a mean of 12.2 minutes to longer than 7 hours intimately depending upon the doses of the antibodies administered (r=0.958). Immunopathological studing showed diffuse deposition of C3 and fibrinogen with a small amount of vascular deposits of rat IgM in the rejected grafts. In the functioning grafts treated with the antibodies, rabbit IgG deposition along endothelium was observed early after transplantation and becam more extensive with toime, while deposits of C3, fibrinogen and rat IgM were minimal. In conclusion, our data suggest that the rabbit antiGP-pAb. at a high dosage prevent the binding of the natural antibodies to the graft endothelium and modulate the complement activation.
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