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Molecular and Clinical Pathological Studies on Atherosclerosis Suppression in the Coronary Artery by Myocardial Bridge.

心肌桥抑制冠状动脉粥样硬化的分子和临床病理学研究。

基本信息

批准号：
12670179
负责人：
ISHII Toshiharu
金额：
$ 1.86万
依托单位：
School of Medicine, Toho University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

项目摘要

The mechanism of atherosclerosis suppression by myocardial bridge(MB) consisting of myocardial tissue which covers a part of the LAD running in the epicardial adipose tissue has been explored from the viewpoints of vascular constriction proteins and coagulation/fibrinolysis proteins in the vascular endothelium and smooth muscle cells altering their expression in accordance with shear stress against the LAD vascular wall.. In addition, the effects of anatomical properties of MB, such as the location of MB within the LAD as well as the length and thickness of MB, on the LAD vascular wall were histomorphometrically investigated.Results1. Intimal thickness beneath MB was significantly lower than that proximal and distal to MB. Furthermore, The expression of e-nitrogen oxide synthase, endothelin-l.angiotensin converting enzyme in endomelium, smooth muscle cells or intimal stroma in the bridged segment was significantly lower there than that proximal and distal to MB.2. In addition to the results of 1, the expression of coagulation/fibrinolysis proteins, such as tissue factor, plasminogen activator-1, tissue plasminogen activator in endothelium, smooth muscle cells or intimal stroma in the bridged segment was also lower significantly than that proximal and distal to MB. The findings of 1 and 2 indicate that the LAD intima beneath the segment of MB was exempt from atherosclerosis development due to the lowering expression of those molecules at the bridged segment.3. By nalysis on the relationship between the anatomical properties, such as the location of MB within the LAD as well as the kength and thickness of MB, and intimal thickness of the LAD, the longer and thicker the anatomical properties of MB were, the greater the effect of atherosclerosis suppression by MB was. The results of 1, 2 and 3 indirectly illustrate that the vascular wall of MB is stressed with higher shear stress than the LAD segments proximal and distal to MB.

从血管内皮细胞和平滑肌细胞中血管收缩蛋白和凝血/纤溶蛋白的表达随着对LAD血管壁的剪切应力而改变的角度，探讨了心肌桥（MB）抑制动脉粥样硬化的机制。心肌桥由覆盖在心外膜脂肪组织中的LAD的一部分的心肌组织组成。此外，通过组织形态计量学方法研究MB在LAD内的位置、长度和厚度等解剖学特性对LAD血管壁的影响。MB下方内膜厚度明显低于MB近端和远端。桥段内膜、平滑肌细胞及内膜基质中e-一氧化氮合酶、内皮素-l、血管紧张素转换酶的表达均显著低于桥段近端和远端.除1的结果外，桥段内皮、平滑肌细胞或内膜间质中的凝血/纤溶蛋白如组织因子、纤溶酶原激活物-1、组织型纤溶酶原激活物的表达也明显低于近端和远端。1和2的结果表明，由于桥连段这些分子的表达降低，MB段下的LAD内膜免于动脉粥样硬化的发展.通过分析MB在LAD内的位置、长度、厚度等解剖学特性与LAD内膜厚度的关系，发现MB的解剖学特性越长、越厚，MB抑制动脉粥样硬化的作用越大。1、2和3的结果间接说明MB的血管壁受到的剪切应力高于MB近端和远端的LAD段。