肿瘤坏死因子诱导的坏死：一种单核细胞介导的高凝效应。
Tumor necrosis factor-induced necrosis: a monocyte-mediated hypercoagulable effect.
作者信息
Spillert C R, Sun S, Ponnudurai R, Miller M A, Lazaro E J
机构信息
Department of Surgery, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103-2757, USA.
出版信息
J Natl Med Assoc. 1995 Jul;87(7):508-9.
The mechanisms by which tumor necrosis factor (TNF) exerts its necrotic effects are somewhat obscure. We hypothesize that TNF, by monocyte activation, produces the procoagulant tissue factor, thus leading to a state of hypercoagulability with resultant thrombotic vascular occlusion and tissue necrosis. To test this hypothesis, modified recalcification time values (in minutes +/- standard deviation) were obtained on aliquots of blood with A) 20 microL of albumin, B) 20 microL of saline containing endotoxin, and C) 20 microL of albumin with 450 units of TNF. No differences were noted if the samples were not incubated. We conclude that TNF, can cause tumor (tissue) necrosis, and since incubation is required, TNF alone (without monocyte activation) has no procoagulant activity.
肿瘤坏死因子（TNF）发挥其坏死作用的机制尚不清楚。我们推测，TNF通过激活单核细胞产生促凝血组织因子，从而导致高凝状态，进而引发血栓性血管闭塞和组织坏死。为了验证这一假设，我们对以下几份血液样本的等分试样测定了修正的复钙时间值（以分钟为单位，±标准差）：A）20微升白蛋白；B）20微升含内毒素的生理盐水；C）20微升含450单位TNF的白蛋白。如果样本不进行孵育，则未观察到差异。我们得出结论，TNF可导致肿瘤（组织）坏死，并且由于需要孵育，单独的TNF（无单核细胞激活）没有促凝血活性。
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