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目的 研究创伤性腹腔内出血血液不凝固的机制。方法 采用Coulter(JT -IR) ,ACL3 0 0 0plus和ELISA分别检测 15例创伤性腹腔内出血病人外周静脉血和腹腔血的血小板计数(PC)、血浆血小板α颗粒膜糖蛋白 14 0 (GMP - 14 0 )、纤维蛋白原 (Fg)和D -二聚体 (D -D)含量。结果 与外周静脉血比较 ,腹腔血中PC和Fg明显减少 (P <0 .0 1)、GMP - 14 0和D -D明显升高 (P<0 .0 1)。结论 创伤性腹腔内出血病人腹腔血中PC和Fg明显减少 ,GMP - 14 0和D -D明显升高 ,提示腹腔血中血小板被激活和破坏增多 ,而且存在继发性纤维蛋白溶解亢进 ,纤维蛋白被降解消耗 ,这可能是腹腔内出血血液不凝固的重要原因。
Objective To study the mechanism of blood coagulation in traumatic intraperitoneal hemorrhage. Methods Peripheral venous blood and peritoneal blood were collected from 15 patients with traumatic intraperitoneal hemorrhage. The platelet count (PC), plasma platelet α - particle glycoprotein 140 (GMP - 14) 0), fibrinogen (Fg) and D-dimer (D-D) content. Results Compared with peripheral venous blood, PC and Fg in peritoneal blood were significantly decreased (P <0.01), GMP - 140 and D - D were significantly increased (P <0.01). Conclusions PC and Fg in the peritoneal blood of traumatic patients with intraperitoneal hemorrhage were significantly decreased, GMP - 140 and D - D were significantly increased, suggesting that platelet activation and destruction increased in the peritoneal blood, with secondary fibrinolytic hyperfunction, fibrin Degraded consumption, which may be an important reason for the non-coagulation of intra-abdominal bleeding blood.