Sakuragawa N, Takahashi K, Shibata A
Adv Exp Med Biol. 1979;120B:185-93.
Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
研究了弥散性血管内凝血(DIC)患者前激肽释放酶的变化,这些DIC患者包括胃癌播散性转移、急性早幼粒细胞白血病和内毒素休克患者。因此,本文的触发物质为白血病病理细胞、培养的高分化腺癌细胞和内毒素。(1)白血病病理细胞和培养细胞的裂解物显示前激肽释放酶激活。内毒素通过因子Ⅻ激活前激肽释放酶。(2)丝氨酸蛋白酶(因子Xa、凝血酶、纤溶酶和胰蛋白酶)激活血浆和纯化的前激肽释放酶中的前激肽释放酶。(3)抗凝血酶Ⅲ、抑肽酶和FOY抑制前激肽释放酶激活。抗凝血酶Ⅲ的抑制作用受肝素促进。