1992 Fiscal Year Final Research Report Summary
Cellular and Molecular Mechanism Coronary Spasm
| 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 KYUSHU UNIVERSITY FACULTY OF MEDICINE Associate Professor, 医学部, 助教授 (90128017)
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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)
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| Project Period (FY) |
1990 – 1992
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| Keywords | coronary artery spasm / endothelium-derived relaxing factor / serotonin / substance P / dysfunction |
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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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