Ishikawa Y, Ishii T, Asuwa N, Masuda S
Department of Pathology, Hachioji Medical Center, Tokyo Medical College, Japan.
Virchows Arch. 1997 Feb;430(2):163-71. doi: 10.1007/BF01008038.
The evolution of atherosclerotic lesions is suppressed in the intima of the human coronary artery, beneath myocardial bridges. To elucidate the mechanism of the protective effect, we investigated morphological changes using the rabbit coronary artery as a model. Rabbit fed a 1%-cholesterol diet were killed at intervals up to 20 weeks. Two short segments of the left coronary arteries running in the epicardial adipose tissue (EpiLAD) and subsequently running in the myocardium (MyoLAD) were compared morphologically. The intima of the EpiLAD had flat endothelial cells with a polygonal shape, and demonstrated raised atherosclerotic lesions with increase in serum cholesterol level. In contrast, the intima of the MyoLAD was free of atherosclerotic lesions throughout the study, and the endothelial cells were spindle-shaped and engorged. While ferritin particles reached only the surroundings of the internal elastic lamina in the MyoLAD, they permeated into the media of the EpiLAD. We suggest that myocardial bridges suppress coronary atherosclerosis by an alteration of endothelial permeability, which may be due to changes in haemodynamic force tending towards a higher shear stress. The data provide an insight into the relationship between haemodynamics and the development of coronary atherosclerosis.
在心肌桥下方的人类冠状动脉内膜中，动脉粥样硬化病变的进展受到抑制。为了阐明这种保护作用的机制，我们以兔冠状动脉为模型研究了形态学变化。给喂食1%胆固醇饮食的兔子每隔一段时间处死，最长至20周。比较了在心外膜脂肪组织中走行（心外膜左冠状动脉，EpiLAD）随后在心肌中走行（心肌内左冠状动脉，MyoLAD）的两段左冠状动脉的形态。EpiLAD的内膜有扁平的多边形内皮细胞，随着血清胆固醇水平升高出现隆起的动脉粥样硬化病变。相比之下，在整个研究过程中，MyoLAD的内膜没有动脉粥样硬化病变，内皮细胞呈纺锤形且肿胀。虽然铁蛋白颗粒仅到达MyoLAD内弹力膜周围，但它们渗透到了EpiLAD的中膜。我们认为，心肌桥通过改变内皮通透性来抑制冠状动脉粥样硬化，这可能是由于血流动力学力倾向于更高切应力的变化所致。这些数据为血流动力学与冠状动脉粥样硬化发展之间的关系提供了见解。
