Peyton B D, Rohrer M J, Furman M I, Barnard M R, Rodino L J, Benoit S E, Hechtman H B, Valeri C R, Michelson A D
Department of Surgery, Center for Platelet Function Studies, University of Massachusetts Medical Center, Worcester 01655, USA.
J Vasc Surg. 1998 Jun;27(6):1109-15; discussion 1115-6. doi: 10.1016/s0741-5214(98)70013-8.
Leukocyte activation has been implicated in the pathogenesis of venous stasis ulceration, but the involvement of activated platelets and leukocyte-platelet aggregates has not been previously investigated. The purpose of this study was to determine whether patients with venous stasis ulceration have increased platelet activation and a propensity toward formation of leukocyte-platelet aggregates.
Blood was drawn from the superficial veins of the leg just proximal to a venous stasis ulcer and from an antecubital vein in 14 patients with venous stasis ulceration. Blood was also drawn from the antecubital vein of 14 volunteers without evidence of venous disease. Whole-blood flow cytometry was used to analyze the samples before and after activation with a panel of agonists for evidence of platelet activation and the formation of leukocyte-platelet aggregates.
Patients with venous stasis ulceration had a greater number of monocyte-platelet aggregates in both the arm and leg samples than did the control subjects (p < 0.01). Furthermore, antecubital blood samples from patients with venous stasis ulceration stimulated with either thrombin-receptor agonist peptide, adenosine diphosphate, or phorbol myristate acetate formed more monocyte-platelet aggregates than did control samples (p < 0.05). No differences in platelet activation or neutrophil-platelet aggregate formation were noted among the three sample groups.
Patients with venous stasis ulceration have an increase in the number of monocyte-platelet aggregates in systemic venous blood as well as in venous blood adjacent to a venous stasis ulcer, implicating the monocyte as the leukocyte involved in the pathogenesis of venous stasis ulceration. No association was identified between the presence of a venous stasis ulcer and either neutrophil-platelet aggregation or the activation of individual platelets. Because platelet activation is necessary for the formation of monocyte-platelet aggregates, these data also suggest that monocyte-platelet aggregation is a more sensitive marker for in vivo platelet activation than is the identification of individual activated platelets.
白细胞活化与静脉淤滞性溃疡的发病机制有关，但活化血小板及白细胞 - 血小板聚集体的参与情况此前尚未得到研究。本研究的目的是确定静脉淤滞性溃疡患者是否存在血小板活化增加以及白细胞 - 血小板聚集体形成倾向。
从14例静脉淤滞性溃疡患者腿部静脉淤滞性溃疡近端的浅静脉及肘静脉采血。还从14名无静脉疾病证据的志愿者的肘静脉采血。使用全血流式细胞术分析样本在用一组激动剂激活前后，以检测血小板活化及白细胞 - 血小板聚集体形成的证据。
静脉淤滞性溃疡患者手臂和腿部样本中的单核细胞 - 血小板聚集体数量均多于对照组（p < 0.01）。此外，用凝血酶受体激动肽、二磷酸腺苷或佛波醇肉豆蔻酸酯刺激的静脉淤滞性溃疡患者的肘静脉血样本比对照样本形成更多的单核细胞 - 血小板聚集体（p < 0.05）。三个样本组之间在血小板活化或中性粒细胞 - 血小板聚集体形成方面未发现差异。
静脉淤滞性溃疡患者全身静脉血以及静脉淤滞性溃疡附近静脉血中的单核细胞 - 血小板聚集体数量增加，这表明单核细胞是参与静脉淤滞性溃疡发病机制的白细胞。未发现静脉淤滞性溃疡的存在与中性粒细胞 - 血小板聚集或单个血小板活化之间存在关联。由于血小板活化是单核细胞 - 血小板聚集体形成所必需的，这些数据还表明，单核细胞 - 血小板聚集比单个活化血小板的识别是体内血小板活化更敏感的标志物。
