Wang C, Kerrigan C L, Stotland M A
Microsurgical Laboratories, Royal Victoria Hospital and McGill University, Montreal, Quebec, Canada.
Plast Reconstr Surg. 1997 Nov;100(6):1482-8; discussion 1489-90. doi: 10.1097/00006534-199711000-00016.
During the ischemia/reperfusion phenomenon, adhesion molecules seem to play a critical role in the recruitment of neutrophils to sites of eventual tissue injury. E-selectin is an endothelium-derived molecule that mediates adhesion of neutrophils to activated endothelial cells. In vitro expression of E-selectin, after exposure to stimuli such as endotoxin, interleukin 1, or tumor necrosis factor alpha is maximal at 4 to 6 h, followed by a decline toward basal levels at 24 to 48 h. Characterizing the temporal expression of E-selectin in an in vivo model of skin flap ischemia-reperfusion would help to determine the optimal approach to eventual pharmacologic blockade. This intervention may prove therapeutically beneficial in attenuating flap injury. This study, using the standard porcine buttock skin flap model, was designed to evaluate immunohistochemically the expression of E-selectin in flaps subjected to (1) arterial ischemia (8 h)-reperfusion (18 h), (2) venous ischemia (8 h)-reperfusion (18 h), and (3) distal ischemia (26 h). Four flaps were examined per group, with 8 biopsies being collected sequentially over the 26-h study period from each flap. Blinded, semi-quantitative histologic scoring revealed the following results: (1) E-selectin is absent in normal porcine skin; (2) with arterial ischemia/reperfusion, E-selectin expression in flaps was maximal at 1 h of reperfusion, declining thereafter; (3) with venous ischemia/reperfusion, E-selectin expression peaked during the first hour of ischemia, with subsequent decline; and (4) within a flap designed to sustain distal ischemia, E-selectin expression is relatively more intense in regions of the flap distant from the vascular pedicle, and maximal at 6 h after flap elevation. Our conclusion, therefore, is that the kinetics of E-selectin expression within the tissues of porcine skin flaps differs depending on the type of ischemic insult sustained. Interpretation of these findings, correlating possible pathophysiologic differences in the different models of ischemia, is offered.
在缺血/再灌注现象中，黏附分子似乎在将中性粒细胞募集到最终发生组织损伤的部位发挥关键作用。E-选择素是一种内皮源性分子，介导中性粒细胞与活化内皮细胞的黏附。在内毒素、白细胞介素1或肿瘤坏死因子α等刺激下，E-选择素的体外表达在4至6小时达到最大值，随后在24至48小时降至基础水平。在皮瓣缺血-再灌注的体内模型中表征E-选择素的时间表达，将有助于确定最终药物阻断的最佳方法。这种干预可能在减轻皮瓣损伤方面具有治疗益处。本研究使用标准的猪臀部皮瓣模型，旨在通过免疫组织化学方法评估E-选择素在经历以下情况的皮瓣中的表达：（1）动脉缺血（8小时）-再灌注（18小时），（2）静脉缺血（8小时）-再灌注（18小时），以及（3）远端缺血（26小时）。每组检查4个皮瓣，在26小时的研究期间从每个皮瓣依次采集8份活检样本。盲法半定量组织学评分显示以下结果：（1）正常猪皮肤中不存在E-选择素；（2）动脉缺血/再灌注时，皮瓣中E-选择素的表达在再灌注1小时时达到最大值，此后下降；（3）静脉缺血/再灌注时，E-选择素表达在缺血的第一小时达到峰值，随后下降；（4）在设计用于维持远端缺血的皮瓣中，E-选择素的表达在皮瓣远离血管蒂的区域相对更强，并在皮瓣掀起后6小时达到最大值。因此，我们的结论是，猪皮瓣组织中E-选择素表达的动力学因所遭受的缺血损伤类型而异。本文还对这些发现进行了解释，并关联了不同缺血模型中可能存在的病理生理差异。
