Cellular and Molecular Mechanism Coronary Spasm

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的动脉粥样硬化兔（WHHL）主动脉内皮源性松弛因子（EFRF）的释放。我们发现动脉粥样硬化血管的松弛减弱是由EFRF的产生受损和EFRF的失活引起的。2)我们研究了皂苷皮血管光滑纤维中Ca^<++>-张力的关系。Ca^<++>-张力关系在痉挛和非痉挛冠状动脉部位切除的制剂中相似。3)在体内研究了EDRF在猪冠状动脉痉挛模型中的作用。EDRF抑制剂（LNNA 1-3 mg/kg）在对照部位增强了5 -羟色胺诱导的收缩，但在痉挛部位没有改变，这表明5 -羟色胺诱导的冠状动脉痉挛不是主要由内皮功能障碍引起的。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的急性进展和急性心肌梗死。3. 我们研究了变异性心绞痛患者的内皮依赖性血管舒张。结果表明，变异性心绞痛患者血管痉挛部位存在P物质引起的内皮依赖性血管舒张。

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.