VASCULAR FLUID-MECHANICS, THE ARTERIAL-WALL, AND ATHEROSCLEROSIS
VASCULAR FLUID-MECHANICS, THE ARTERIAL-WALL, AND ATHEROSCLEROSIS
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DOI：
10.1115/1.2891384
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发表时间：
1992-08-01
影响因子：
1.7
通讯作者：
NEREM, RM
中科院分区：
文献类型：
--
作者：
NEREM, RM
动脉粥样硬化是一种大中型动脉疾病，在美国和大多数西方世界是主要的死亡原因。严重的动脉粥样硬化干扰血流；然而，即使在疾病的早期阶段，即在动脉粥样硬化形成期间，疾病过程与动脉中的血流特征之间也被认为是重要的关系。动脉粥样硬化的发生涉及许多因素之间相互作用的复杂级联。其中包括流体机械因素，据信这是该病高度集中的一个原因。从活体研究中，有证据表明血流动力学对血管内皮细胞、内膜增厚和单核细胞募集有影响。此外，细胞培养研究已经证明了细胞的机械环境对结构和功能的重要影响。这些证据大多针对内皮细胞，它被认为是任何血液动力学效应的关键中介，现在已经很好地记录了培养的内皮单层在流体施加的层流剪应力的响应下，在结构和功能上经历了各种变化。尽管近年来取得了进展，但仍有许多领域的进一步工作将提供重要的新信息。其中之一是对细胞培养环境进行工程设计，使其更具生理性。动物研究在我们理解动脉粥样硬化形成的努力中也是必不可少的，显然我们需要更好的信息来了解疾病的模式及其在人类和动物模型中的时间发展，以及特定的潜在生物事件。作为补充，动脉流体力学的体外模型研究将是补充。此外，人们可以预见，在我们努力了解动脉粥样硬化形成过程的病理生理学过程中，计算机模拟将发挥越来越大的作用。这不仅包括计算流体力学，还包括对动脉壁内发生的病理生物学过程进行建模。动脉粥样硬化形成过程的关键可能在于了解血流动力学如何不仅影响内膜平滑肌细胞的增殖，而且影响单核/巨噬细胞的募集和泡沫细胞的形成。最后，有必要开始将我们对细胞现象的知识整合到对动脉壁内生物过程的描述中，然后将其整合到疾病过程本身的图景中。
Atherosclerosis, a disease of large- and medium-size arteries, is the chief cause of death in the United States and in most of the western world. Severe atherosclerosis interferes with blood flow; however, even in the early stages of the disease, i.e. during atherogenesis, there is believed to be an important relationship between the disease processes and the characteristics of the blood flow in the arteries. Atherogenesis involves complex cascades of interactions among many factors. Included in this are fluid mechanical factors which are believed to be a cause of the highly focal nature of the disease. From in vivo studies, there is evidence of hemodynamic influences on the endothelium, on intimal thickening, and on monocyte recruitment. In addition, cell culture studies have demonstrated the important effect of a cell's mechanical environment on structure and function. Most of this evidence is for the endothelial cell, which is believed to be a key mediator of any hemodynamic effect, and it is now well documented that cultured endothelial monolayers, in response to a fluid flow-imposed laminar shear stress, undergo a variety of changes in structure and function. In spite of the progress in recent years, there are many areas in which further work will provide important new information. One of these is in the engineering of the cell culture environment so as to make it more physiologic. Animal studies also are essential in our efforts to understand atherogenesis, and it is clear that we need better information on the pattern of the disease and its temporal development in humans and animal models, as well as the specific underlying biologic events. Complementary to this will be in vitro model studies of arterial fluid mechanics. In addition, one can foresee an increasing role for computer modelling in our efforts to understand the pathophysiology of the atherogenic process. This includes not only computational fluid mechanics, but also modelling the pathobiologic processes taking place within the arterial wall. A key to the atherogenic process may reside in understanding how hemodynamics influences not only intimal smooth muscle cell proliferation, but also the recruitment of the monocyte/macrophage and the formation of foam cells. Finally, it will be necessary to begin to integrate our knowledge of cellular phenomena into a description of the biologic processes within the arterial wall and then to integrate this into a picture of the disease process itself.