| Project/Area Number |
25670761
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HAYAKAWA Koichi 関西医科大学, 医学部, 助教 (60403086)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 循環障害 / 壁応力 / 腸管 / 敗血症 / 臓器血流 / 組織血流 / 組織応力 |
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| Outline of Final Research Achievements |
The present study was performed to clarify the relationship between wall stress and mucosal perfusion of the gut with or without experimental sepsis in rabbits. Increase in wall stress up to 12 mmHg by intramural drip infusion of normal saline did not significantly alter mucosal perfusion of the small intestine evaluated by using Laser Doppler surface scanning (Moor LDI). Intravenous administration of endotoxin (E.coli O111, dissolved in normal saine at 1 mg/mL) at the dosage of 1 mg/kg significantly decreased mean arterial pressure, mucosal perfusion of the small intestine at 60, 90min after the administration of endotoxin, but did not alter the wall stress of the small intestine by 120min. These results suggest that vasoactive mediators released during sepsis seem to play more significant role in circulatory disturbance of the intestinal mucosa than that of increased intestinal wall stress due to pathological edema formation.
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