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Relationship between the evolution of coronary artery spasm and atherosclerosis and related basic studies on the mechanisms of coronary spasm

冠状动脉痉挛的演变与动脉粥样硬化的关系及冠状动脉痉挛机制的相关基础研究

基本信息

批准号：
61440042
负责人：
NAKAMURA Motoomi
金额：
$ 17.92万
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：
1986
资助国家：
日本
起止时间：
1986 至 1987
项目状态：
已结题

项目摘要

1. Mechanisms of Coronary Arterial Spasm in Experimental Animal Model Endothelial balloon denudation of the coronary artery was performed under fluoroscopy in miniature pigs and the animals were fed laboratory chow for 3 months, after which coronary artery spasm was repeatedly provoked by histamine given intracoronarily. To evaluate coronary artery spasm without the influence of blood constituents and neural control and to quantitate the pharmacophysiological characteristics of histamine-induced coronary hyperconstriction, the same heart was isolated and perfused with Krebs-Henseleit solution under a constant perfusion pressure of 90 mmHg. Focally potentiated constriction of the coronary artery to histamine was reproducible in isolated pig hearts perfused with electrolyte solution containing 2.6 mM Ca^<2+>. The constriction of the denuded areas in response to histamine was topologically the same in vivo and in vitro. Alterations in the influx of Ca^<2+> in the presence of H_1-receptor stiumulation in vascular smooth muscle of the vessel with intimal thickening was suggested as a plausible mechanism of coronary spasm.2. Cellular Mechanisms of Ca^<2+> Handling in Cultured Smooth muscle Cell Changes in the concentration of cytosolic free calcium were recorded microfluorometrically in rat vascular smooth muscle cells in primary culture and loaded with quin-2. Transient elevations of calcium repeatedly appeared in response to both repetitive depolarization (100 mM K^+) and caffeine (19 mM) applications with progressive reductions in peak levels. Quantitative analysis of released calcium suggested that caffeine- and depolarization-sensitive intracellular calcium strage sites is identical.

1.实验动物模型中冠状动脉痉挛的机制在荧光透视下对小型猪进行冠状动脉内皮球囊剥脱术，并给动物喂实验室食物3个月，之后冠状动脉内给予组胺反复引起冠状动脉痉挛。为了评价冠状动脉痉挛而不受血液成分和神经控制的影响，并定量组胺诱导的冠状动脉过度收缩的药理生理学特征，分离同一心脏，并在90 mmHg的恒定灌注压下用Krebs-Henseleit溶液灌注。在用含2.6 mM Ca^<2+>的电解质溶液灌注的离体猪心中，组胺引起的冠状动脉局灶性增强收缩是可重复的。收缩的裸露区域在组胺的反应是拓扑相同的在体内和体外。结论：1.在H_1受体激活的情况下，血管平滑肌细胞内Ca^<2+>内流的改变可能是冠状动脉痉挛的一个可能机制.培养的平滑肌细胞中Ca^2+处理的细胞机制在原代培养的大鼠血管平滑肌细胞中用荧光显微镜记录细胞溶质游离钙浓度的变化，并用quin-2加载。在重复去极化（100 mM K^+）和咖啡因（19 mM）的作用下，钙离子的瞬时升高反复出现，峰值水平逐渐降低。释放钙的定量分析表明，咖啡因和去极化敏感的细胞内钙的strage网站是相同的。