TY - T1的脑缺血再灌注损伤和粘附JF -神经学乔-神经病学SP - S23 LP - S26做- 10.1212 / WNL.49.5首页_Suppl_4。S23六世- 49 -生理4非盟-雷蒙德·j·Winquist盟史蒂文克尔Y1 - 1997/11/01 UR - //www.ez-admanager.com/content/49/5_Suppl首页_4/S23.abstract N2 -提示再灌注缺血组织恢复正常功能至关重要,但它可以沉淀的渐进破坏可逆受损细胞,导致矛盾的组织功能障碍和坏死。这个再灌注损伤多因子的病因,但与白细胞的呵斥的渗透,随后释放细胞毒性介质,在先前缺血性组织。1、2早期再灌注过程中的事件是中性粒细胞的粘附和积累。虽然这是预期作为治疗过程的一部分,它可以大声斥责由于血管内皮激活的炎症介质如血小板激活因子(PAF)参谋长和活性氧代谢产物。中性粒细胞的积累,加上红细胞和血小板,会导致毛细管plugging3和微血管血流量的减少,导致停滞的病灶部位。一旦渗透到组织中,中性粒细胞能够释放各种蛋白酶,lipid-derived介质,和活性氧伤害潜在可挽回的细胞。中性粒细胞的粘附和迁移是由几个策划类的细胞表面糖蛋白。其中包括白细胞整合蛋白(CD11 / CD18)、免疫球蛋白超基因家族(细胞间粘附molecule-1 (ICAM-1);血管细胞粘附molecule-1 (VCAM-1)],和selectins (L - P -,和E-selectin)。4研究采用单克隆抗体(mab)针对特定成员的各种途径帮助证明中性粒细胞在缺血再灌注损伤的重要性。 In the heart, studies by Simpson et al.5 (anti-CD11b) and Seewaldt-Becker et al.6 (anti-CD11a, anti-CD18, anti-ICAM-1) were among the first to demonstrate that MAbs directed against either leukocyte or endothelial cell adhesion glycoproteins were effective in limiting the myocardial necrosis that developed in response to an ischemia-reperfusion protocol. Efficacy has also been demonstrated for MAbs administered just before reperfusion directed against the following molecules: L- … ER -