Endotoxin-induced Wistar Rat Model Of DIC And Urokinase Intervention

Objective: 1. To establish the endotoxin-induced DIC Wistar rat model 2. To explore intervention effect of uroldnase in endotoxin-induced DIC Wistar rat model.Methods: Wistar rats 60 Only, female, weight 160～170g, Weeks 6-7 weeks. 1, endotoxin-induced DIC Wistar rat model: meet the test criteria of Wistar rats were randomly assigned to the experimental group and control group. pentobarbital (30mg/kg) by intraperitoneal anesthesia, by tail vien 2.5ml/h infusion of saline or endotoxin 3mg/kg/h, after respectively 1, 2, 4 hours took the abdominal vein blood sample. EDTA and 3.8% sodium citrate for anticoagulation, made the detection of PT, APTT, FIB, ALT, Cr, PAI- 1 and D-dimer, platelet counts under the microscope. Live Donor rat kidney, liver and lung specimens, 10% formalin-fixed, embedded, sectioned. HE, MSB and PTAH stain was followed. 2, urokinase intervention methods: meet the test criteria of Wistar rats were randomly assigned to the experimental group and controled group, respectively by tail vien intravenous of saline (NS), urokinase (UK), lipopolysaccharide (LPS) and urokinase + endotoxin (UK+LPS group)×4 hours. Anesthesia, abdominal venous blood sample, liver, kidney, lung specimens agree with the former.Results: 1, endotoxin-induced DIC Wistar rat model results: Wistar rats by LPS (3mg/kg/h) concentrations were imported via the tail vein 1 hour, 2 hours, 4 hours, it can be seen that the plasma PT, APTT gradually extended, PLT, FIB gradually reduced, ALT, Cr gradually increased, both reached the peak two hours, four hours to the state platform. Fibrinolysis, PAI- 1 and D-dimer levels began to rise significantly, with PAI- 1 was increased further, D-dimer decline. Liver, kidney, lung biopsy showed cell degeneration, swelling, which can be seen microvascular fibrin microthrombi formation, The change in a minor-hour, two hours and four hours most obvious. It was associated with focal hemorrhage. Fibrin Micro thrombosis was most easy to see in glomerular. This model suggested when made importation LPS of an hour it starts the signs of DIC, with the extension of time infusion, DIC performance increasingly obvious. 2, urokinase intervention trials indicated: (1). after urokinase intervention, PT, APTT value may not return to the NS controlled group, but more significantly shorten than LPS group, and PLT, FIB little change, the level of PAI- 1 concentrations was reduce, and D-dimer levels were significantly increased. (2). the urokinase intervention group, Cr and ALT significantly lower than controlled group. The liver, kidney, lung biopsy showed: the urokinase intervention group tissue injury than LPS group reduced, glomerular fibrin formation rate has declined markedly. (3). Experimental process indicated: LPS group did 4 of 10 deaths, died of respiratory failure, respectively Urokinase and intervention group for only one of tenth death.Conclusion: (1) We first make the establishment of DIC model successfully induced by the endotoxin (3mg/kg/h)in Wistar rats. (2) This study showed that urokinase could improve LPS-induced DIC Wistar rat model of abnormal coagulation and fibrinolysis, organ dysfunction positively. (3)whether the UK will be able to reduce the LPS-induced DIC Wistar rat model of mortality, it need to expand the sample for further observation.