| Project/Area Number |
13671344
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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 |
Digestive surgery
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
YUKIOKA Tetsuo Tokyo Medical University, Medicine, Professor, 医学部, 教授 (00182668)
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| Co-Investigator(Kenkyū-buntansha) |
本間 宙 東京医科大学, 医学部, 助手 (60307353)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Gut / ischemia-reperfusion / NO / 一酸化窒素 / 虚血再還流障害 / 虚血再灌障害 / NO / ARDS / Gut translocation |
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| Research Abstract |
BACKGROUND : The nature of the involvement of an inducible nitric oxide (NO) release in acute conditions has been controversial. We sought to determine whether a relatively selective inducible NO synthase inhibitor, aminooguanidine (AG), ameliorates pulmonary microvascular injury after gut ischemia -reperfusion. METHODS : Anesthetized Wistar rats underwent superior mesenteric artery occlusion for 30 mm and reperfusion for 6 hr (I/R) or sham operation (SHAM). Another set of animals undergoing I/R received an aminoguanidine IP (I/R+AG). Pulmonary vascular permeability was assessed by measuring tissue retention of Evans blue, a dye that binds albumin (EBD). RESULTS : The concentrations of NO_2/NO_3 (lung and plasma) in the I/R group were higher than those of the sham (p<0.01). The lung/plasma EBD ratio In the I/R group was also higher than that of the sham. Treatment with the aminoguanidine prevented this lung injury induced by the gut isehemia-reperfusion. CONCLUSION : Increased lung vascular permeability elicited by gut I/R was significantly attenuated with inhibition of an inducible NO release by AG.
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