Dietrich W D, Dewanjee S, Prado R, Watson B D, Dewanjee M K
Department of Neurology, University of Miami School of Medicine, FL 33101.
Stroke. 1993 Oct;24(10):1534-40. doi: 10.1161/01.str.24.10.1534.
Thromboembolic events are a major cause of ischemic stroke. To obtain evidence for platelet embolization after cerebrovascular injury, the accumulation of indium-labeled platelets was documented after photothrombosis of the rat common carotid artery.
Heterologous blood was collected from donor rats, and the isolated platelets were labeled with 111In-tropolone. Labeled platelets were then infused into Wistar rats 30 minutes before right carotid artery thrombosis. Nonocclusive common carotid artery thrombosis was induced by a laser-driven rose bengal-mediated photochemical insult to the vascular endothelium, and the rats were killed 15 minutes or 3 hours later. Carotid arteries and brains were immediately removed and dissected for regional radioactivity assessment or sectioned for the autoradiographic visualization of platelet emboli.
At 15 minutes after thrombosis, the ratio of right-to-left common carotid artery radioactivity was significantly elevated compared with control (33 +/- 12 [mean +/- SEM] versus 0.97 +/- 0.2). Within individual brain regions, including the frontal and frontoparietal cortices and hippocampus, significant elevations in right-to-left radioactivity ratios were also documented. Autoradiographic images revealed multiple foci of 111In-labeled platelets throughout the thrombosed hemisphere. At the level of the frontal cortex, bilateral platelet accumulation was seen. Regional counts demonstrated significantly increased platelet density within selective cortical and subcortical regions. In contrast to the 15-minute findings, right-to-left ratios of carotid arteries or brain regional radioactivities were not significantly elevated at 3 hours after injury. In addition, the areal densities of autoradiographically visualized platelets in the 3-hour group were not different from control except in the right frontal cortex.
These data demonstrate (1) the acute accumulation of labeled platelets in downstream vessels after nonocclusive common carotid artery thrombosis, (2) that platelet accumulation is widespread and also involves contralateral areas, and (3) that platelet accumulation within the thrombosed carotid artery and brain is largely transient.
血栓栓塞事件是缺血性卒中的主要病因。为获取脑血管损伤后血小板栓塞的证据，在大鼠颈总动脉光血栓形成后记录铟标记血小板的聚集情况。
从供体大鼠采集异体血，分离的血小板用111In - 托酚酮标记。标记后的血小板于右侧颈动脉血栓形成前30分钟注入Wistar大鼠。通过激光驱动孟加拉玫瑰红介导的光化学损伤血管内皮诱导非闭塞性颈总动脉血栓形成，15分钟或3小时后处死大鼠。立即取出颈动脉和脑，进行区域放射性评估或切片以进行血小板栓子的放射自显影观察。
血栓形成后15分钟，右侧与左侧颈总动脉放射性比值与对照组相比显著升高（33±12[均值±标准误]对0.97±0.2）。在包括额叶、额顶叶皮质和海马体在内的各个脑区，右侧与左侧放射性比值也有显著升高。放射自显影图像显示在血栓形成的半球内有多个111In标记血小板的聚集点。在额叶皮质水平，可见双侧血小板聚集。区域计数显示在选择性皮质和皮质下区域血小板密度显著增加。与15分钟时的结果相反，损伤后3小时颈动脉或脑区放射性的右侧与左侧比值未显著升高。此外，除右侧额叶皮质外，3小时组放射自显影观察到的血小板面密度与对照组无差异。
这些数据表明：（1）非闭塞性颈总动脉血栓形成后标记血小板在下游血管中急性聚集；（2）血小板聚集广泛且累及对侧区域；（3）血栓形成的颈动脉和脑内的血小板聚集在很大程度上是短暂的。
