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SAH后CVS的发生和发展是受痉挛血管周围的血液刺激启动的,这包括血管内皮细胞功能的紊乱。痉挛血管内皮细胞壁上有明显的ICAM-1的上调,且与血管的痉挛程度密切相关。ICAM-1介导白细胞粘附到血管内皮细胞,并透过内皮屏障迁移到组织中。ICAM-1介导的血管壁的炎症反应在SAH后CVS的病理生理过程中起了重要作用,而应用抗ICAM-1单克隆抗体进行治疗可以有效缓解CVS的程度。
The occurrence and development of CVS after SAH is triggered by blood stimulation around the vasospasm vessels, which includes the disturbance of the function of vascular endothelial cells. Spasm vascular endothelial cell wall obvious ICAM-1 upregulation, and with the degree of vascular spasm are closely related. ICAM-1 mediates leukocyte adhesion to vascular endothelial cells and migrates into the tissue through the endothelial barrier. ICAM-1-mediated inflammation of the vascular wall plays an important role in the pathophysiology of CVS after SAH, whereas the treatment with anti-ICAM-1 monoclonal antibody can effectively reduce the extent of CVS.