Dietrich W D, Prado R, Halley M, Watson B D
Department of Neurology, University of Miami School of Medicine, FL 33101.
J Neuropathol Exp Neurol. 1993 Jul;52(4):351-60. doi: 10.1097/00005072-199307000-00002.
The microvascular and neuronal consequences of nonocclusive common carotid artery (CCA) thrombosis were documented in rats. Thrombosis of the CCA was produced by a rose bengal-mediated photochemical insult and regional patterns of blood-brain barrier (BBB) disruption were documented by horseradish peroxidase (HRP) histochemistry at 15 min (n = 12), 4 h (n = 3), 1 day (n = 5) or 7 days (n = 5) after vascular injury. At 15 min and 4 h after thrombosis, multiple foci of BBB disruption were present throughout the thrombosed hemisphere; protein leakage was occasionally detected contralaterally. Extravasated HRP was associated with well-perfused arterioles and arterioles containing luminal platelet aggregates at different stages of degranulation. Evidence for local platelet adhesion and aggregation or endothelial disruption at these sites was not detected. However, HRP-containing endothelial plasmalemmal vesicles were present at leaky sites. Variable degrees of parenchymal injury were documented including dendritic and astrocytic swelling with neuronal necrosis. By 1 day after CCA thrombosis, the overall frequency of permeable sites, more commonly associated with luminal leukocytes and parenchymal necrosis, was reduced. At 7 days, vessels permeable to HRP were associated with tissue necrosis, reactive astrocytes and microglial infiltration. Arteriole wall thickening and leukocyte accumulation within arterioles and venules were also detected. Widespread platelet embolization leading to variable degrees of BBB disruption and tissue injury occurs after CCA thrombosis. Acute abnormalities in vascular permeability are thus hypothesized to play an important role in the acute pathogenesis of cerebrovascular thrombosis. Delayed leukocyte accumulation in this model of embolic infarction may represent a secondary insult to the injured brain.
在大鼠中记录了非闭塞性颈总动脉（CCA）血栓形成的微血管和神经元后果。通过孟加拉玫瑰红介导的光化学损伤产生CCA血栓形成，并在血管损伤后15分钟（n = 12）、4小时（n = 3）、1天（n = 5）或7天（n = 5），用辣根过氧化物酶（HRP）组织化学记录血脑屏障（BBB）破坏的区域模式。在血栓形成后15分钟和4小时，整个血栓形成的半球出现多个BBB破坏灶；偶尔在对侧检测到蛋白质渗漏。外渗的HRP与灌注良好的小动脉以及含有处于不同脱颗粒阶段的管腔内血小板聚集体的小动脉相关。在这些部位未检测到局部血小板粘附、聚集或内皮破坏的证据。然而，在渗漏部位存在含HRP的内皮细胞质膜小泡。记录了不同程度的实质损伤，包括树突和星形胶质细胞肿胀伴神经元坏死。在CCA血栓形成后1天，与管腔内白细胞和实质坏死更常见相关的可渗透部位的总体频率降低。在7天时，对HRP可渗透的血管与组织坏死、反应性星形胶质细胞和小胶质细胞浸润相关。还检测到小动脉壁增厚以及小动脉和小静脉内白细胞积聚。CCA血栓形成后发生广泛的血小板栓塞，导致不同程度的BBB破坏和组织损伤。因此，推测血管通透性的急性异常在脑血管血栓形成的急性发病机制中起重要作用。在这个栓塞性梗死模型中，白细胞的延迟积聚可能代表对受损脑的继发性损伤。
