Ratnoff O D, Emanuelson M M, Ziats N P
Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio.
J Clin Invest. 1987 Oct;80(4):1180-9. doi: 10.1172/JCI113177.
Suspensions of peripheral blood mononuclear cells (PBMC), monocytes, T or B lymphocytes, platelets or granulocytes, and cell-depleted supernatant fluids of these suspensions inhibited activation of Hageman factor (HF, Factor XII) by ellagic acid, a property not shared by erythrocytes. PBMC also inhibited HF activation by glass or sulfatides. Contaminating platelets may have contributed to inhibition by PBMC. Elaboration of agents inhibiting HF activation required metabolically active cells. The inhibitor(s) in PBMC supernates were not identified with known agents, but had properties of a nonenzymatic protein. PBMC supernates did not contain fibrinogen, nor alter the thrombin, prothrombin, or partial thromboplastin times of normal plasma, amidolysis by activated plasma thromboplastin antecedent (Factor XIa) or activated Stuart factor (Factor Xa) or esterolysis by C1 (C1 esterase); they inhibited plasmin minimally. These experiments suggest that peripheral blood cells may impede intravascular coagulation. Whether this property helps maintain the fluidity of blood is unclear.
外周血单核细胞（PBMC）、单核细胞、T或B淋巴细胞、血小板或粒细胞的悬浮液，以及这些悬浮液去除细胞后的上清液，均可抑制鞣花酸对Hageman因子（HF，凝血因子XII）的激活作用，而红细胞则无此特性。PBMC还可抑制玻璃或硫脂对HF的激活作用。PBMC的抑制作用可能与其中污染的血小板有关。抑制HF激活的物质的产生需要代谢活跃的细胞。PBMC上清液中的抑制剂不是已知物质，但具有非酶蛋白的特性。PBMC上清液中不含纤维蛋白原，也不改变正常血浆的凝血酶、凝血酶原或部分凝血活酶时间，不影响活化血浆凝血活酶前体（凝血因子XIa）的酰胺水解作用或活化Stuart因子（凝血因子Xa）的酰胺水解作用，也不影响C1（C1酯酶）的酯解作用；它们对纤溶酶的抑制作用极小。这些实验表明外周血细胞可能会阻碍血管内凝血。这种特性是否有助于维持血液的流动性尚不清楚。
