创伤性腹腔内出血血液不凝机制的研究

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）,ＡＣＬ３０００ｐｌｕｓ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１４０（ＧＭＰ－１４０）、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〈０．０１）、ＧＭＰ－１４０和Ｄ－Ｄ明显升高（Ｐ〈０．０１

Study on Blood Incoagulable Mechanism of Traumatic Intraperitoneal Hemorrhage

Objective To study the blood incoagulable mechanism of traumatic intraperitoneal hemorrhage. Methods Platelet count (PC), GMP-140, Fibrinogen (Fg) and D-Dimer (D-D) in both the peripheral venous blood and the intraperitoneal blood were measured in 15 patients with traumatic intraperitoneal hemorrhage by Coulter (JT-IR), ACL 3000 plus and ELISA. Results It was found that PC and Fg of the intraperitoneal blood were remarkably decreased in comparison with those of the peripheral blood ( P <0.01), but GMP-140 and D-D were remarkably increased ( P <0.01). Conclusions In the intraperitoneal blood of the patients with traumatic intraperitoneal hemorrhage, PC and Fg decrease, but GMP-140 and D-D increase, which indicates that platelets are activated and over consumed, and fibrinogen is degraged. There is secondary fibrinolysis in the intraperitoneal blood. It may be the important reason for blood incoagulation in traumatic intraperitoneal hemorrhage.