| Project/Area Number |
17590726
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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 |
Circulatory organs internal medicine
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
MATSUMOTO Tetsuya Shiga University of Medical Science, Department of Cardiovascular and Respiratory Medicine, Assistant Professor, 医学部, 講師 (70273406)
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| Co-Investigator(Kenkyū-buntansha) |
URADE Yoshihiro Osaka Bioscience Institute, Head, 研究部長 (10201360)
EGUCHI Yutaka Shiga University of Medical Science, Intensive Care Unit, Professor, 医学部, 教授 (00263054)
HONE Minoru Shiga University of Medical Science, Department of Cardiovascular and Respiratory Medicine, Professor, 医学部, 教授 (90183938)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Prostaglandin D2 / Atherosclerosis / Coronary artery / Smooth muscle / coronary / prostagiandin / atheroscierosis / prostaglandin |
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| Research Abstract |
Lipocalin-type prostaglandin D synthase (L-PGDS) catalyzes the biosynthesis of prostaglandin D_2 (PGD2), which acts as an anticoagulant, vasodilaor, and inflammatory mediator. We hypothesized that L-PGDS has clinical impact on the genesis of coronary vasospasm. Thus, we examined serum L-PGDS levels, coronary macro-and microvasomotor function, and their relationship in 96 patients with chest pain and angiographically normal coronary arteries. Methods : Acetylcholine (ACh) at increasing doses (3, 10, 30, 100 μg/min) was infused into the left coronary artery, and the diameter and blood flow of the left anterior descending coronary artery (LAD) were analyzed by quantitative angiography and Doppler guide wire examination. The serum L-PGDS level prior to angiography was determined by the ELISA method. Results : Infusion of ACh induced coronary vasospasm of the LAD in all patients with coronary vasospastic angina (CSA), but in none of the patients with chest pain (CP) syndrome. ACh caused marginal vasoconstriction in the CP group, but produced dose-dependent constrictions of LAD arteries in the CSA group. Coronary vasodilations induced by 0.25 mg of nitoroglycerin or increases in coronary blood flow induced by 12 mg of papaverine did not differ between the two groups. There were no significant differences in baseline clinical characteristics between the CP and CSA groups, except for the frequency of smoking. Serum L-PGDS levels in the CSA group were significantly higher than those in the CP group. Correction of smoking status yielded similar results. Significant negative correlations were observed between the degrees of LAD vasomotion in response to ACh (3, 10, 30 μg/min) and serum L-PGDS levels. Serum L-PGDS levels did not correlate with coronary vasomotions induced by nitoroglycerin or papaverine.
Conclusion : L-PGDS may be a predictor of coronary vascular reactivity in patients with CSA.
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