| Project/Area Number |
11671503
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | KAGWA MEDICAL UNIVERSITY |
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Principal Investigator |
OGURA Shinji Kagawa Medical University, Hospital, Assistant professor, 附属病院, 助教授 (30185566)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | Gram-positive bacteria / shock / sepsis / anti-thrombin III / tyrosine kinase / cytokine / GBS / antithrombin III / 敗血症性ショック / Tyrosine / Shock / Seplic Shock / LPS |
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| Research Abstract |
To clear the mechanisms of beneficial effect of antithrombin III (ATIII) on septic shock, we have investigated rat shock model induced by cecal ligation puncture (CLP). Animals subjected to CLP exhibited severe shock with a mean survival time of 15.6 hours, and finally all animals expired. ATIII treated animals simultaneously with CLP significantly prolonged survival and 50% of the rats survived. CLP increased serum IL-6 concentration remarkably at 2, 4, 8 hours after the start of experiment. ATIII significantly decreased the cytokine production. To investigate the direct cellular effects of ATIII, rat peritoneal macrophages were collected and harvested as previously described. Adherent cells were stimulated with either Endotoxin (LPS) or heat killed group B streptococcus (GBS) in the presence or absence of ATIII.IL-6 production from macrophages was activated with LPS and GBS, whereas ATIII inhibited the increase. IL-2 production was slightly increased from the control but ATIII did not affect the production. These results indicate that ATIII may have beneficial effects on rat shock, possibly by blocking inflammatory cytokine production directly.
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