| Project/Area Number |
13671723
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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 |
Obstetrics and gynecology
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| Research Institution | Ehime University |
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Principal Investigator |
OCHI Hiroshi Ehime University, University Hospital, Associate Professor, 医学部附属病院, 助教授 (50194569)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Keiichi Ehime University, University hospital, Lecturer, 医学部附属病院, 講師 (80263937)
TOMIHIRO Katayama Ehime University, School of Medicine, Instructor, 医学部, 助手 (90304625)
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| Project Period (FY) |
2001 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Periventricular Leukomalacia / Microcirculation / Cytokine / Angiotensin / Arteriole / 脳室周囲白質周囲軟化症 / 接着反応 / ヘムオキシゲナーゼ / パワートプラ / 血管抵抗 |
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| Research Abstract |
A progressive relationship was noted between increasing TNF-α levels and increased risk of neonatal periventricular leukomalacia. The purpose of this study was to determine the changes in cerebral vascular reactivity to vasoactive substances in the cerebral arteriole of normal rats indeuced by intraperitoneal administration of TNF-α.
Cerebral arterioles were observed by intravital microscopy assisted by a video imager with cranial window method. We determined the cerebral vascular reactivity to norepinephrine (NE) (0.01〜10 μg/kg/min) and angiotensin II (AT II) (0.01〜10 μg/kg/min) in normal rats. Furthermore, we evaluated the changes in cerebral vascular reactivity to AT-II (1μg/kg/min) indeced by intraperitoneal administration of TNF-α (25μg/kg).
The administration of 0.01, 0.1, 1, 10 μg/kg/min NE induced dose-dependent arteriolar vasoconstriction. Maximum vasoconstriction of 29±14% was attained at a concentration of 10 μg/kg/min NE. On the other hand, the administration of 0.01, 0.1, 1, 10 μg/kg/min AT II did not induced significant arteriolar vasoconstriction. A significant change in cerebral vascular reactivity to AP II was observed after intraperitoneal administration of TNF-α. Vasoconstriction of 7±5% in control group was increased to 23±14% in TNF-α administered group (p<0.05).
Our data suggest that cerebral arterial response to AT II is different from the response to NE, and TNF-α modulates cerebral arterial response to AT-II.
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