Stehbens W E
Lancet. 1975 Mar 29;1(7909):724-7. doi: 10.1016/s0140-6736(75)91633-5.
An experimental model of atherosclerosis sheep veins identical to the human disease indicates (i) that ingestion of an atherogenic diet is not a prerequistie in atherosclerosis and (ii) that haemodynamic stress must be the dominant aetiological factor in atherosclerosis. Ultrastructural studies reveal that the early lipid deposition in spontaneous human atherosclerosis and in haemodynamically induced atherosclerosis is related to the trasnformation of extracellular vesicular debris into closely packed membranous profiles with electron-translucent centres. It is postulated that the vesicular dtsintegration of mural cells is due to the same haemodynamic stresses which induce degenerative changes in the vascular connective tissues, and that the lipid accumulation within the vesicular disintegration of mural cells is due to the same haemodynamic stresses which induce degenerative changes in the vascular connective tissues, and that the lipid accumulation within the vesicular debris is a cellular debris which have not undergone resolution or phagocytosis.
（i）摄入致动脉粥样硬化饮食并非动脉粥样硬化的先决条件；（ii）血流动力学应激必定是动脉粥样硬化的主要病因。超微结构研究显示，自发性人类动脉粥样硬化和血流动力学诱导的动脉粥样硬化中早期脂质沉积与细胞外囊泡碎片转化为具有电子透明中心的紧密堆积膜状结构有关。据推测，壁细胞的囊泡解体是由诱导血管结缔组织退行性变化的相同血流动力学应激所致，并且壁细胞囊泡解体内的脂质积累是由于诱导血管结缔组织退行性变化的相同血流动力学应激，而囊泡碎片内的脂质积累是尚未经历溶解或吞噬作用的细胞碎片。
