| Project/Area Number |
02404045
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
KOYANAGI Samon (1991-1992) KYUSHU UNIVERSITY FACULTY OF MEDICINE Associate Professor, 医学部, 助教授 (90128017)
丸岡 雄二 (1990) 九州大学, 医学部, 助手 (10190563)
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| Co-Investigator(Kenkyū-buntansha) |
SUEISHI Katsuo KYUSHU UNIVERSITY FACULTY OF MEDICINE Professor, 医学部, 教授 (70108710)
IMAIZUMI Tsutomu KYUSHU UNIVERSITY FACULTY OF MEDICINE Lecturer, 医学部, 講師 (60148947)
KANAIDE Hideo KYUSHU UNIVERSITY FACULTY OF MEDICINE Professor, 医学部, 教授 (80038851)
砂川 賢二 九州大学, 医学部, 講師 (50163043)
稲生 哲治 九州大学, 医学部, 講師 (10159965)
小柳 左門 九州大学, 医学部, 講師 (90128017)
友池 仁暢 九州大学, 医学部, 助教授 (90112333)
竹下 彰 九州大学, 医学部, 教授 (30038814)
中村 元臣 中村学園大学, 大学院栄養科学研究科, 教授 (60037322)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥30,700,000 (Direct Cost: ¥30,700,000)
Fiscal Year 1992: ¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 1991: ¥13,300,000 (Direct Cost: ¥13,300,000)
Fiscal Year 1990: ¥10,000,000 (Direct Cost: ¥10,000,000)
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| Keywords | coronary artery spasm / endothelium-derived relaxing factor / serotonin / substance P / dysfunction / coronary spasm / endothelium / substaucep / 冠攣縮 / 内皮細胞依存性血管弛緩因子 / 動脈硬化 / セロトニン / サブスタンスP / 冠動脈攣縮 / 心筋虚血 / Ca^<2+>ーカイネティックス / Ca^<2+>チャネル / 血管内皮細胞依存性弛緩 |
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| Research Abstract |
1.Factors that mediate hypercontraction of atherosclerotic blood vessels
1) We measured the release of endothelium-derived relaxing factor (EFRF) from aorta of hypercholesterolemic atherosclerotic rabbit (WHHL) using a bioassay technique. We found that attenuated relaxation of the atherosclerotic vessels resulted from both an impaired production of EFRF and inactivation of EFRF.
2) We studied Ca^<++>-tension relationship in saponin-skinned vascular smooth fibers. The Ca^<++>-tension relationship was similar in preparations excised from the spastic and non-spastic coronary artery site.
3) We studied the role of EDRF in the cause of coronary spasm in the swine model in vivo. An inhibitor of EDRF (LNNA 1-3 mg/kg) potentiated serotonin-induced constriction at the control site, but did not alter it in the spastic site, suggesting that serotonin-induced coronary spasm did not resulted primarily from endothelial dysfunction. 2. We examined whether intense coronary spasm causes progression of coronary stenosis in our swine model, and found that coronary spasm of abrupt onset resulted in acute progression of organic stenosis and acute myocardial infarction. 3. We studied endothelium-dependent vasodilation in patients with variant angina. The results indicated that endothelium-dependent vasodilation evoked with substance P was present at the vasospastic site in patients with variant angina.
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