| Project/Area Number |
23792086
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
SUMI YUKA 順天堂大学, 医学部, 准教授 (40403084)
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| Research Collaborator |
KURODA Youko 順天堂大学, 男女共同参画室, 派遣社員
JUNGER Wolfgang Harvard大学, 教授
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ATP / 炎症反応 / 好中球 / CD11ｂ / 心肺蘇生後 / 敗血症 / SIRS / 炎症 / ミトコンドリア / adenosine / 虚血再灌流障害 / アデノシン三リン酸 / 全身性炎症反応症候群 / CD11b |
|---|
| Research Abstract |
In systemic inflammatory syndrome response (SIRS) patients, plasma ATP levels were significantly higher than healthy controls (HC). Among SIRS, in post cardiac arrest syndrome (PCAS) patients, that whole-body ischemic reperfusion injury causes inflammation, plasma ATP was higher in non-survivors compared to survivors and HC. Besides, the ATP levels in PCAS correlate with APACHE score. In sepsis patients, neutrophil activation (CD11b expression) was significantly higher than in HC and the mean florescence intensity of CD11b correlates with plasma ATP. These data suggest that ATP release from damaged cells or activated inflammatory cells stimulates neutrophils via ATP receptors and triggers inflammation in SIRS.
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