2007 Fiscal Year Final Research Report Summary
Introduction of prostacyclin synthase gene for treatment of cerebral vasospasm
| Project/Area Number |
17591500
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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 |
Cerebral neurosurgery
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| Research Institution | Gunma University |
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Principal Investigator |
YOSHIDA Takaaki Gunma University, Faculty Medicine, Assistant Professor (40375572)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Nobuhito Tokyo University, Hospitoal, Professor (60262002)
TAKAHASHI Akio Gunma University, Faculty of Medicine, Associate Professor (60261856)
IMAI Hideaki Gunma University, Faculty of Medicine, Assistant Professor (70359587)
KAZAMA Ken Gunma University, Graduete school of Medicine, Assistant Professor (30396626)
SUZUKI Tomonari Saitama Medical University, Schcol of Medicine, Assistant Professor (50361374)
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| Project Period (FY) |
2005 – 2007
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| Keywords | subarachnoid hemorrhege / cerebral vasospasm / ischemic tention recording / Prostacyclin |
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| Research Abstract |
Cerebral vasospasm is a severe complication of subarachnoid hemorrhage that frequently arises after rupture of a cerebral aneurysm, but the pathogenesis is still unclear. Cerebral vasospasm is a unique clinical phenomenon characterized by the delayed and prolonged contraction of the major cerebral arteries. subarachnoid hemorrhage causes dysfunction of endothelium, and inhibition of endothelium-derived relaxing factor. Then, restoration of endothelium derived relaxing factor may treat the phenomenon. The representative endothelium-derived relaxing factor is NO. Introduction of NO synthetase gene treat cerebral vasospasm in experimental SAH model. We paid attention to another endothelium-derived relaxing factor, prostacycline (PGI2), and tested pharmacological effect of PGI2 (beraprost sodium) using isometric tension recording. The beraprost sodium could not inhibit the contraction induced by high dose potassium (80mM). And, that could not inhibit the contraction induced by 100 μmol/L norepinephrine, too. The beraprost sodium 10, 100 μmol/L, 1 mmol/L could inhibit the contraction induced by 10 μmol/L PGF2α, dose-dependently. However, the contractile inhibition effect of beraprost sodium might not be sufficient for the treatment of cerebral vasospasm after SAH. Then, We thought it difficult that introduction of PGI2 synthetase gene had a great inihibitory effect to the severe cerebral vasoconstriction after SAH. PGI2 may have a possibility to be new therapeutic agent for cerebral vasospasm, however the further studies were required.
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