Scannell G, Waxman K, Vaziri N D, Zhang J, Kaupke C J, Jalali M, Hect C
Department of Surgery, University of California-Irvine, USA.
J Trauma. 1995 Oct;39(4):641-4. doi: 10.1097/00005373-199510000-00004.
During traumatic injury, a multitude of events, including ischemia, may cause leukocyte adhesion and margination. In this study, alterations of surface receptors involved in leukocyte adhesion were studied in traumatized patients. In an attempt to discern the role of hypoxia, additional experiments were conducted in which normal human leukocytes were subjected to hypoxic stress in vitro.
Venous blood was obtained from 10 trauma patients within 2 hours of blunt injury (mean Injury Severity Score of 17 +/- 8) and from 8 normal volunteers (controls). Leukocytes were isolated from patients and controls. To assess the effect of hypoxia, normal leukocytes were placed in hermetically sealed environments containing 100% nitrogen. All leukocytes were labeled with phycoerythrin- or fluorescein-bound monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1), or to integrins CD18 and CD11b. Receptor concentration was measured by flow cytometry. Results were expressed as percentage of receptor-positive cells (%) and mean fluorescence channel units, which directly correlate with monoclonal antibody cell surface density. Significance of differences was tested by analysis of variance/Kruskal-Wallis test.
Compared with the normal controls, circulating leukocytes obtained from traumatized patients showed decreased expression of ICAM-1, CD11b, and CD18 2 hours after injury. In contrast, normal leukocytes exposed to hypoxic stress in vitro exhibited a marked increase in CD11b and CD18 expression and no change in ICAM-1 expression.
Leukocytes obtained from traumatized patients showed a significant decrease in cell surface expression of adhesion receptors. This phenomenon is unlikely to be a direct consequence of hypoxia alone, because exposure to isolated hypoxia in vitro actually increased expression of CD11b and CD18.
在创伤性损伤期间，包括局部缺血在内的多种事件可能导致白细胞黏附和靠边。在本研究中，对创伤患者中参与白细胞黏附的表面受体变化进行了研究。为了试图明确缺氧的作用，还进行了额外实验，将正常人白细胞置于体外低氧应激环境中。
在钝性损伤后2小时内从10名创伤患者（平均损伤严重度评分为17±8）和8名正常志愿者（对照组）采集静脉血。从患者和对照组中分离白细胞。为评估缺氧的影响，将正常白细胞置于含100%氮气的密封环境中。所有白细胞均用藻红蛋白或荧光素结合的抗细胞间黏附分子-1（ICAM-1）、整合素CD18和CD11b单克隆抗体进行标记。通过流式细胞术测量受体浓度。结果以受体阳性细胞百分比（%）和平均荧光通道单位表示，这与单克隆抗体细胞表面密度直接相关。差异的显著性通过方差分析/克鲁斯卡尔-沃利斯检验进行检验。
与正常对照组相比，创伤患者伤后2小时的循环白细胞显示ICAM-1、CD11b和CD18的表达降低。相反，体外暴露于低氧应激的正常白细胞显示CD11b和CD18表达显著增加，而ICAM-1表达无变化。
创伤患者的白细胞显示黏附受体的细胞表面表达显著降低。这种现象不太可能仅是缺氧的直接后果，因为体外单独暴露于缺氧环境实际上增加了CD11b和CD18的表达。
