| Project/Area Number |
62570699
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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 |
麻酔学
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| Research Institution | GUNMA UNIVERSITY |
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Principal Investigator |
GOTO Fumio GUNMA UNIVERSITY SCHOOL OF MEDICINE, 医学部, 助教授 (00092015)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Platelet activating factor / Endotoxin shock / Leukotriene / Vascular permeability / 血小板活性化因子拮抗薬 / 白血球 |
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| Research Abstract |
Platelet activating factor (PAF) produces shock in animals and has been implicated in the pathogenesis of experimental endotoxin shock. LTs have also been suggested as key mediators in a number of pathologic processes including vasopermeability and cardiac dysfunction. These two substances have also strong interaction in their synthetic pathway and biological activities. We have studied the effect of specific PAF receptor antagonists (CV-3988,CV-6208) and LTs antagonists (FPL-55712,ONO-1708) on endotoxin-induced systemic reactions and survival rate in rats. Pretreatment with CV or FPL did not prevent the change of plasma transaminase, platelet count and hematocrit following the administration of lipopolisaccharide (LPS), and it did not improve the survival rate from endotoxin shock. On the contrary, combined pretreatments of CV and FPL or ONO improved significantly the survival rates and pre-vented the increase of hematocrit following LPS administration.
Four days after the administation of vinblastine (VB), white blood cell count decreased to 1200 220/mm^3. In the rats that received VB, survival rate increased significantly and prevent the change of plasma transaminase following the adminstration of LPS. These findings suggest that PAF and LT released from the white blood cells may play a pivotal role in the pathogenesis of endotoxin shock and are closely related to the hemodynamic change and vascular permeability.
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