Tagami M, Nara Y, Kubota A, Sunaga T, Maezawa H, Fujino H, Yamori Y
Stroke. 1987 Jul-Aug;18(4):733-40. doi: 10.1161/01.str.18.4.733.
We studied ultrastructurally cerebral perforating arteries in 60 stroke-prone spontaneously hypertensive rats (SHRSP), which were sequentially killed at 4-52 weeks of age before showing symptoms of stroke. Another 24 SHRSP were killed soon after they showed symptoms of cerebral infarction. The initial vascular lesions observed in the asymptomatic group included focal cytoplasmic necrosis in the outer layers of the media. This change progressed to widespread medial necrosis with time. In the infarction group, numerous monocytes were seen adhering to the endothelium of the arteries having advanced medial damage. Following the adherence of monocytes to the endothelium, large amounts of plasma components were visible in the arterial wall. The accumulation of the plasma components (especially fibrin) thickened the wall, narrowed the lumen, and resulted in occlusion. These results suggest that monocytes may affect the endothelium, perhaps disturbing the so-called blood-brain barrier to proteins. The monocytes may therefore be closely related to the occurrence of arterial occlusion with resultant cerebral infarction.
我们对60只易患中风的自发性高血压大鼠(SHRSP)的脑穿通动脉进行了超微结构研究,这些大鼠在出现中风症状前于4至52周龄时被依次处死。另外24只SHRSP在出现脑梗死症状后不久被处死。在无症状组中观察到的初始血管病变包括中膜外层的局灶性细胞质坏死。随着时间的推移,这种变化发展为广泛的中膜坏死。在梗死组中,可见大量单核细胞附着于中膜严重受损的动脉内皮。单核细胞附着于内皮后,动脉壁中可见大量血浆成分。血浆成分(尤其是纤维蛋白)的积聚使血管壁增厚、管腔狭窄并导致阻塞。这些结果表明,单核细胞可能会影响内皮,也许会干扰所谓的蛋白质血脑屏障。因此,单核细胞可能与导致脑梗死的动脉阻塞的发生密切相关。