Sadoshima S, Fukushima T, Tanaka K
Stroke. 1979 Jul-Aug;10(4):411-4. doi: 10.1161/01.str.10.4.411.
Thirty-nine thrombosed arterial segments of the branches of the circle of Willis were studied by a complete serial section technique. Twenty-two patients had been hypertensive and 8 had hypercholesterolemia before the onset of cerebral artery thrombosis. The histological characteristics of the thrombosed arterial segments were intramural hemorrhage in 28 segments, superficial edema of the fibrous cap of the atheroma of fibrous plaque in 4, rupture of the atheromatous plaque in 1, superficial accumulation of foam cells in the atheroma in 1 and an atheroma or fibrous plaque without any other changes in 5. They were many intramural small blood vessels in the atheroma or fibrous plaques of 22 segments with intramural hemorrhage. Fibrinoid degeneration of these small blood vessels was noted in 5. These findings suggested that intramural hemorrhage from the intramural small blood vessels was the major cause of cerebral artery thrombosis and that persistent hypertension not only promoted cerebral atherosclerosis but also induced hemorrhage from the intramural small blood vessels.
采用完整连续切片技术对39个 Willis 环分支的血栓形成动脉节段进行了研究。22例患者在脑动脉血栓形成前患有高血压，8例患有高胆固醇血症。血栓形成动脉节段的组织学特征为：28个节段有壁内出血，4个节段纤维斑块动脉粥样硬化的纤维帽有表面水肿，1个节段动脉粥样斑块破裂，1个节段动脉粥样硬化中有泡沫细胞表面聚集，5个节段有动脉粥样硬化或纤维斑块但无任何其他变化。在22个有壁内出血的节段的动脉粥样硬化或纤维斑块中有许多壁内小血管。其中5个节段的这些小血管有纤维蛋白样变性。这些发现表明，壁内小血管的壁内出血是脑动脉血栓形成的主要原因，持续高血压不仅促进脑动脉粥样硬化，还诱导壁内小血管出血。
