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Cellular and Molecular Mechanism Coronary Spasm

冠状动脉痉挛的细胞和分子机制

基本信息

批准号：
02404045
负责人：
KOYANAGI Samon
金额：
$ 19.65万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (A)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1992
项目状态：
已结题

项目摘要

1.Factors that mediate hypercontraction of atherosclerotic blood vessels1) 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.

1.介导动脉粥样硬化血管过度收缩的因素1)我们使用生物测定技术测量了高胆固醇血症动脉粥样硬化兔(WHHL)主动脉内皮衍生舒张因子(EFRF)的释放。我们发现动脉粥样硬化血管的松弛减弱是由于EFRF产生受损和EFRF失活造成的。2)我们研究了皂苷皮血管平滑纤维中的Ca^++-张力关系。 Ca^++-张力关系在从痉挛性和非痉挛性冠状动脉部位切除的制剂中是相似的。3)我们在体内猪模型中研究了EDRF在引起冠状动脉痉挛中的作用。 EDRF 抑制剂（LNNA 1-3 mg/kg）增强了对照部位的 5-羟色胺诱导的收缩，但在痉挛部位没有改变它，这表明 5-羟色胺诱导的冠状动脉痉挛并非主要由内皮功能障碍引起。 2.我们在猪模型中检查了剧烈的冠状动脉痉挛是否会导致冠状动脉狭窄的进展，发现突然发作的冠状动脉痉挛会导致器质性狭窄和急性心肌梗死的急性进展。 3. 我们研究了变异型心绞痛患者的内皮依赖性血管舒张作用。结果表明，变异型心绞痛患者的血管痉挛部位存在 P 物质诱发的内皮依赖性血管舒张。