Davenport W D, Ball C R
Atherosclerosis. 1981 Oct;40(2):145-52. doi: 10.1016/0021-9150(81)90032-0.
A semipurified diet containing 28% fat (as lard), but no known atherogenic substances such as cholesterol, was fed to a group of Swiss stock mice. A group of similar mice was fed laboratory chow as controls. Within six weeks of diet feeding, experimental mice developed atrial thrombosis. In scattered areas of atria where thrombi were not present, the scanning electron microscope showed an endothelial response to the high-fat diet in the form of holes and crater-like lesions. In extreme cases, a whole endothelial cell might be almost totally destroyed. Clusters of leucocytes mixed with platelets and fibrin attached to the larger holes, suggesting the initiating mechanism of thrombogenesis, were also observed.
给一组瑞士种小鼠喂食一种半纯化饮食，该饮食含28%的脂肪（以猪油形式），但不含胆固醇等已知致动脉粥样硬化物质。另一组相似的小鼠喂食实验室普通饲料作为对照。在喂食饮食六周内，实验小鼠出现了心房血栓形成。在心房中未出现血栓的散在区域，扫描电子显微镜显示内皮细胞对高脂饮食有孔和火山口样病变形式的反应。在极端情况下，整个内皮细胞可能几乎完全被破坏。还观察到与血小板和纤维蛋白混合的白细胞簇附着在较大的孔上，提示这是血栓形成的起始机制。
