Zivelin A, Rao L V, Rapaport S I
Department of Medicine, University of California, San Diego, La Jolla, USA.
Blood Cells Mol Dis. 1995;21(1):9-19. doi: 10.1006/bcmd.1995.0003.
Adherence and aggregation of leukocytes within the vessels of a prepared skin site has been shown to be essential for the pathogenesis of the local Shwartzman reaction (LSR) (Argenbright and Barton: J Clin Invest 89: 259, 1992). We have now performed experiments in rabbits to evaluate whether coagulation within the vessels of a prepared site is a second requirement for the reaction. Skin sites were prepared by an intradermal injection of endotoxin 24 hours before a provoking intravenous injection of endotoxin. Thirteen control rabbits all developed the LSR. Seven of 12 rabbits given warfarin to achieve anticoagulation approximating that used therapeutically in humans before the provoking injection were protected against the LSR (p = 0.003). Five of nine rabbits given anti-rabbit factor X IgG before the provoking injection to yield mean values in individual rabbits of between 7% and 18% plasma factor X activity were protected against the LSR (p = 0.009). Six of 11 rabbits given anti-rabbit factor VII IgG before the provoking injection to yield mean values in individual rabbits of between < 0.5% and 2.2% were protected against the LSR (p = 0.007). Four rabbits failed to develop the LSR at an endotoxin-prepared skin site when an infusion of tissue factor (TF) causing substantial intravascular coagulation was substituted for a provoking injection of endotoxin. It would appear that two events are required for the pathogenesis of the LSR provoked by endotoxin: formation of aggregated masses of WBC in the prepared skin vessels and deposition of fibrin due to TF-initiated coagulation.
在已制备的皮肤部位血管内白细胞的黏附和聚集已被证明是局部施瓦茨曼反应（LSR）发病机制的关键因素（阿金布赖特和巴顿：《临床研究杂志》89：259，1992）。我们现在在兔子身上进行了实验，以评估已制备部位血管内的凝血是否是该反应的第二个必要条件。在静脉注射内毒素引发反应前24小时，通过皮内注射内毒素来制备皮肤部位。13只对照兔均出现了LSR。12只在引发注射前给予华法林以达到近似人类治疗用量的抗凝效果的兔子中，有7只受到保护未出现LSR（p = 0.003）。9只在引发注射前给予抗兔因子X IgG以使个体兔子血浆因子X活性平均值在7%至18%之间的兔子中，有5只受到保护未出现LSR（p = 0.009）。11只在引发注射前给予抗兔因子VII IgG以使个体兔子平均值在<0.5%至2.2%之间的兔子中，有6只受到保护未出现LSR（p = 0.007）。当用导致大量血管内凝血的组织因子（TF）输注替代引发注射的内毒素时，4只兔子在由内毒素制备的皮肤部位未出现LSR。内毒素引发的LSR发病机制似乎需要两个事件：在已制备的皮肤血管中形成白细胞聚集团块以及由于TF启动的凝血导致纤维蛋白沉积。
