Parmley W W, Blumlein S, Sievers R
Am J Cardiol. 1985 Jan 25;55(3):165B-171B. doi: 10.1016/0002-9149(85)90627-7.
The process of atherosclerosis, although not completely understood, is being clarified. A unifying hypothesis holds that the initial event is endothelial injury, followed by platelet aggregation and release reactions. This leads to smooth muscle cell migration into the intima and replication, with subsequent secretion of elastin, collagen and glycosaminoglycans (which binds lipids). Several animal studies have shown that calcium plays an important role in this process. Many drugs with diverse properties can inhibit experimental atherosclerosis. These drugs appear to reduce intracellular calcium. The calcium-channel blockers nifedipine, diltiazem and verapamil, which decrease intracellular calcium, also protect animals from experimental atherosclerosis. The relevance of these animal models to human atherosclerosis is uncertain, and there are very few studies concerning regression of atherosclerosis by interfering with calcium fluxes. Further studies will be needed to clarify these points.
动脉粥样硬化的过程虽然尚未完全明了，但正在逐步得到阐明。一个统一的假说是，初始事件为内皮损伤，随后是血小板聚集和释放反应。这会导致平滑肌细胞迁移至内膜并增殖，随后分泌弹性蛋白、胶原蛋白和糖胺聚糖（可结合脂质）。多项动物研究表明，钙在这一过程中起重要作用。许多具有不同特性的药物可抑制实验性动脉粥样硬化。这些药物似乎能降低细胞内钙水平。钙通道阻滞剂硝苯地平、地尔硫䓬和维拉帕米可降低细胞内钙水平，也能保护动物免受实验性动脉粥样硬化的影响。这些动物模型与人类动脉粥样硬化的相关性尚不确定，而且关于通过干扰钙通量使动脉粥样硬化消退的研究非常少。需要进一步研究来阐明这些问题。
