PLATELET AND LEUKOCYTE ADHESION IN THE MICROVASCULATURE AT THE CEREBRAL SURFACE IMMEDIATELY AFTER SUBARACHNOID HEMORRHAGE
PLATELET AND LEUKOCYTE ADHESION IN THE MICROVASCULATURE AT THE CEREBRAL SURFACE IMMEDIATELY AFTER SUBARACHNOID HEMORRHAGE
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DOI：
10.1227/01.neu.0000337579.05110.f4
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发表时间：
2009-03-01
期刊：
影响因子：
4.8
通讯作者：
Watanabe, Eiju
中科院分区：
文献类型：
--
作者：
Ishikawa, Mami;Kusaka, Gen;Watanabe, Eiju
目的：蛛网膜下腔出血（SAH）后的病理生理学尚未得到很好的研究。本研究的目的是使用体内颅窗法观察血小板-白细胞-内皮细胞相互作用作为SAH急性期炎症和促血栓形成反应的指标。方法：使用血管内穿孔法诱导C57 Bl/6 j小鼠蛛网膜下腔出血。活体显微镜用于监测用不同荧光染料标记的血小板和白细胞的滚动和粘附。激光多普勒血流仪测定局部脑血流量。观察SAH后30 min、2 h、8 h血小板-白细胞-内皮细胞相互作用。在SAH后2小时检测P-选择素抗体和烟酰胺腺嘌呤二核苷酸磷酸氧化酶抑制剂apocynin对这些反应的影响，并与将自体血液注入到枕大孔中的不同SAH模型进行比较。SAH伴有60%的局部脑血流量下降，而对侧局部脑血流无变化。SAH引起脑小静脉中滚动和粘附的血小板和白细胞的时间和大小依赖性增加。所有这些相互作用减弱治疗与P-选择素抗体或夹竹桃麻素。有没有显着的血细胞招聘中观察到的血液注射SAHmodel.CONCLUSION：SAH在颅底诱导P-选择素和氧自由基介导的血小板-白细胞-内皮细胞在脑表面的微静脉的相互作用。这些早期的炎症和促血栓形成反应可能在SAH后立即引起全脑损伤。
OBJECTIVE: Pathophysiology after subarachnoid hemorrhage (SAH) caused by aneurysmal rupture has not been well examined. The purpose of this study was to observe platelet-leukocyte-endothelial cell interactions as indexes of inflammatory and prothrombogenic responses in the acute phase of SAH, using an in vivo cranial window method.METHODS: Subarachnoid hemorrhage was induced in C57Bl/6j mice by using the endovascular perforation method. Intravital microscopy was used to monitor the rolling and adhesion of platelets and leukocytes that were labeled with different fluorochromes. Regional cerebral blood flow was measured with laser Doppler flowmetry. The platelet-leukocyte-endothelial cell interactions were observed 30 minutes, 2 hours, and 8 hours after SAH. The effect of P-selectin antibody and apocynin, an inhibitor of nicotinamide adenine dinucleotide phosphate oxidase, on these responses was examined at 2 hours after SAH, and compared with a different SAH model in which autologous blood was injected into the foramen magna.RESULTS: SAH was accompanied by a 60% decrease in regional cerebral blood flow, whereas no changes in regional cerebral blood flow were observed on the contralateral side. SAH elicited time- and size-dependent increases in rolling and adherent platelets and leukocytes in cerebral venules. All of these interactions were attenuated by treatment with a P-selectin antibody or apocynin. There was no significant blood cell recruitment observed in the blood-injected SAH model.CONCLUSION: SAH at the skull base induced P-selectin- and oxygen radical-mediated platelet-leukocyte-endothelial cell interactions in venules at the cerebral surface. These early inflammatory and prothrombogenic responses may cause a whole-brain injury immediately after SAH.