Role of leucocytes in damage to the vascular endothelium during ischaemia-reperfusion injury
Role of leucocytes in damage to the vascular endothelium during ischaemia-reperfusion injury
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DOI：
10.1080/09674845.2006.11732743
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发表时间：
2006-01-01
影响因子：
1.9
通讯作者：
Adams, R. A.
中科院分区：
文献类型：
--
作者：
Hughes, S. F.;Cotter, M. J.;Adams, R. A.
本研究采用止血带诱导前臂缺血再灌注损伤模型，探讨白细胞在缺血再灌注损伤过程中对血管内皮的损伤作用。白细胞诱捕是通过测量离开手臂的静脉血中白细胞的浓度来研究的。中性粒细胞和单核白细胞亚群分离密度梯度离心技术。流式细胞术检测细胞表面CD11b的表达和细胞内过氧化氢的产生。采用酶联免疫吸附测定（ELISA）技术测定血浆弹性酶和血管性血友病因子（vWF）浓度。缺血再灌注时，中性粒细胞（P=0.040）和单核细胞表面CD11b表达升高（P=0.049），外周血白细胞表面CD11b表达降低（P=0.019）。白细胞亚群胞内过氧化氢生成增加（P=0.027[中性粒细胞]，P=0.091[单核细胞]），血浆弹性酶浓度增加（P=0.05）。血浆vWF浓度也有升高的趋势（P=0.0562）， vWF是内皮损伤的标志。缺血-再灌注导致白细胞黏附性、包裹性和活化性增加。即使在轻度缺血性损伤后，这种白细胞反应也会立即出现内皮损伤的迹象。这些结果可能对理解涉及轻度缺血发作的慢性疾病的发展具有重要意义。
During this investigation, a model of tourniquet-induced forearm ischaemia-reperfusion injury is employed to investigate the role of leucocytes in damage to the vascular endothelium during ischaemia-reperfusion injury. Leucocyte entrapment is investigated by measuring the concentration of leucocytes in venous blood leaving the arm. Neutrophil and monocyte leucocyte subpopulations are isolated by density gradient centrifugation techniques. Cell surface expression of CD11b and the intracellular production of hydrogen peroxide are measured via flow cytometry. Plasma concentrations of elastase and von Willebrand factor (vWF) are measured using enzyme-linked immunosorbernt assay (ELISA) techniques. During ischaemia-reperfusion, there was an increase in CD11b cell surface expression on neutrophils (P=0.040) and monocytes (P=0.049), and a decrease in peripheral blood leucocytes (P=0.019). There was an increase in the intracellular production of hydrogen peroxide by leucocyte subpopulations (P=0.027 [neutrophils], P=0.091 [monocytes]) and in the plasma elastase concentration (P=0.05). There was also a trend to increasing plasma concentration of vWF (P=0.0562), which was measured as a marker of endothelial damage. Ischaemia-reperfusion results in increased adhesiveness, entrapment and activation of leucocytes. Even following a mild ischaemic insult, this leucocyte response was followed immediately by evidence of endothelial damage. These results may have important implications for understanding the development of chronic diseases that involve mild ischaemic episodes.