2007 Fiscal Year Final Research Report Summary
Small diameter vascular prosthesis with anti-clotting and anti-inflammatory response
Project/Area Number |
18591417
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General surgery
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Research Institution | Ehime University |
Principal Investigator |
SHIOZAKI Takahiro Ehime University, University Hospital, Assistant Professor (40419510)
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Co-Investigator(Kenkyū-buntansha) |
IMAGAWA Hiroshi Ehime University, Graduate School of Medicine, Associate Professor (90273622)
KAWACHI Kenji Ehime University, Graduate School of Medicine, Professor (90116020)
TSUNOOKA Nobuo Ehime University, Graduate School of Medicine, Senior Assistant Professor (10380239)
TAKAHASHI Manabu Ehime University, Graduate School of Science and Engineering, Associate Professor (20274334)
OGI Keiji Ehime University, Graduate School of Science and Engineering, Professor (70281194)
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Project Period (FY) |
2006 – 2007
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Keywords | small caliber grafts / angiotensin II / angiotensin II type 1 recentor blacker. ARB |
Research Abstract |
Preserving endothelial function of arterial conduits may affect early and long-term patency of small caliber grafts. Mechanism of angiotensin II-induced endothelial dysfunction is not well understood. So we evaluated the in vitro effects of angiotensin II and valsartan (angiotensin II type 1 receptor blocker, ARB) on the endothelium dependent relaxation of aortic ring from wister rats. The aortas which were excised in anesthetized rats cut into ring segments. Each ring was incubated for 24 h at 37℃ in Dulbecco's modified Eagle's medium containing 0.5% calf serum with or without angiotensin II and valsartan. Using an organ bath technique, contractile responses to 80mmol/L KCl and 300nmol/L phenylephrine were evaluated. And relaxation responses were examined using sodium nitroprusside (10^<-11> to 10^<-7>mol/L) or acetylcholine (10^<-9> to 10^<-5> mol/L) after contraction by 300nmol/L phenylephrine. Contractile response to phenylephrine was potentiated by angiotensin II (100nmol/L). Angiotensin II (100nmol/L) responded to sodium nitroprusside, but impaired relaxations to acetylcholine. However, adding valsartan responded to acetylcholine. The endothelium-dependent relaxation of the aorta by means of valsartan was improved. We conclude that Varsartan improved the endothelium-dependent relaxation of the aorta in rats that received angiotensin II.
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