BACKGROUND: After multiple trauma, blood coagulation activity is enhanced and fibrinolytic activity is suppressed by overproduction of plasminogen activator inhibitor-1 (PAI-1). Intermittent sequential pneumatic compression (ISPC) is an effective method to prevent deep vein thrombosis. Its action is explained by the mechanical effect on blood flow, as well as by the enhancement of fibrinolysis by the reduction of PAI-1. The aim of this study was to determine the effects of ISPC on coagulation and fibrinolysis after multiple trauma. METHODS: Thirty-nine trauma patients were either treated with ISPC (ISPC group, 20 patients) or without ISPC (control group, 19 patients). We measured the plasma levels of the thrombin antithrombin III complex (TAT), the plasmin alpha 2 plasmin inhibitor complex (PIC), the tissue plasminogen activator (t-PA), and the plasminogen activator inhibitor-1 (PAI-1) on admission and at 1, 2, 3, 6, 12, and 24 hours after admission. RESULTS: The TAT was higher than normal in both groups, with no significant difference between the two groups throughout the study period. The PIC level of ISPC group was significantly higher than that of the control group. In the ISPC group, the PIC level increased gradually, reaching a peak at 3 hours and decreasing thereafter. In the control group, the PIC level increased to a peak level at 2 hours. The TAT/PIC ratio dropped in the first two hours and increased at 3 hours, dropping again thereafter. In the ISPC group, the ratio dropped gradually without an intermittent fluctuation. At 3 and 6 hours, the control group showed a significantly greater ratio compared to the ISPC group. PAI-1 was higher than normal in bothgroups, with a significantly lower level in the ISPC group from 2 hours to 24 hours. For the t-PA level, no difference was noted between the two groups, with the peak level occurring at 1 hour. The PAI-1/t-PA ratio was significantly greater in the control group from 2 hours to 12 hours than in the ISPC group, but the difference was not significant at 24 hours. CONCLUSIONS: In multiple trauma patients, ISPC does not seem to affect coagulation, but enhances fibrinolysis through suppressed PAI-1 production. This effect of ISPC may be maintained for 12 hours.
alpha-2-Antiplasmin ; Antithrombin III ; Blood Coagulation ; Fibrinolysin ; Fibrinolysis* ; Humans ; Multiple Trauma* ; Plasma ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Thrombin ; Tissue Plasminogen Activator ; Venous Thrombosis

BACKGROUND: After multiple trauma, blood coagulation activity is enhanced and fibrinolytic activity is suppressed. Due to high tissue thromboplastin concentration in cerebral tissue, more serious coagulation and fibrinolytic abnormalities may occur when concomitant head trauma is present. The aim of this study was to determine the changes in coagulation and fibrinolysis after trauma and the effects of head trauma on coagulation and fibrinolysis. METHODS: This study includes 35 trauma patients: 16 patients with head trauma (group A) and 19 patients without head trauma (group B). We measured the plasma levels of functional protein C, antithrombin III (AT III), thrombin antithrombin III complex (TAT), plasmin alpha 2 plasmin inhibitor complex (PIC), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 antigen (PAI-1) on admission and on days 1, 2, 4, and 6 after the trauma. RESULTS: The TAT and the TAT/PIC were significantly higher in group A than in group B on all days. PIC was significantly lower in group A than in group B on all days except the day of admission. Over the course of time, the TAT and the TAT/PIC decreased in both groups and PIC increased. On admission, the PAI-1 of both groups was increased, but it decreased over the course of time. The t-PA was increased on admission, was suppressed on the 1st day, and then increased again. The PAI-1 and the t-PA showed no significant difference between the two groups. CONCLUSIONS: After multiple trauma, coagulation was enhanced and fibrinolysis was suppressed. Enhanced coagulation and suppressed fibrinolysis were significantly greater in group A than in group B.
alpha-2-Antiplasmin ; Antithrombin III ; Blood Coagulation ; Craniocerebral Trauma ; Fibrinolysin ; Fibrinolysis* ; Humans ; Multiple Trauma* ; Plasma ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Protein C ; Thrombin ; Thromboplastin ; Tissue Plasminogen Activator

PURPOSE: The object of present study was to investigate the relationship between LCPD and the abnormality of certain plasma proteins affecting clot mechanism and fibrinolysis in patients with LCP disease. MATERIALS AND METHODS: Twenty-five consecutive patients who had been diagnosed as LCP disease were matched with twenty-five controls for gender, age (2-year range) , and the time of presentation (1-year range) . There were twenty-three boys and two girls. The mean age of the children when the LCP disease was diagnosed was 6.7 years ( range, 2.1-12.8 years) , and the mean age at the time of the present study was 7.9 years ( range, 3.4 - 13 year) . Thrombotic disorders were investigated for protein C activity/antigenicity, protein S activity/antigenicity, antithrombin III, anticardiolipin antibody Ig G, anticardiolipin antibody Ig M, lupus antibody. Fibrinolytic disorders were investigated for tissue type plasminogen activator (t-PA) , plasminogen, plasminogen activator inhibitor-1 (PAI-1) , alpha 2 plasmin inhibitor, lipoprotein (a) . Wilcoxon rank sum test was used for the comparison. RESULTS: There was no significant difference in coagulation system and fibrinolytic system between patients and controls. CONCLUSION: Our results suggest that abnormality in coagulation and fibrinolytic system is not associated with Legg-Calv -Perthes disease.
alpha-2-Antiplasmin ; Antibodies, Anticardiolipin ; Antithrombin III ; Blood Proteins ; Child ; Female ; Fibrinolysis ; Humans ; Lipoprotein(a) ; Plasminogen ; Plasminogen Activators ; Protein C ; Protein S ; Thrombophilia* ; Tissue Plasminogen Activator

To easily obtain plasmin-alpha(2)-antiplasmin complex (PAP) with high purity, the purification procedure was improved by authors. After urokinase activated fresh human platelet-deficient plasma had been applied to Lysine-Sepharose 4B affinity chromatography column, elutions were sequentially performed by several eluents with different ingredients. The results showed that 3.0 mg PAP could harvested from 100 ml fresh plasma by this method and the whole procedure could be finished within several hours. In conclusion, this procedure is simple, rapid, economical and high-yield.
Blotting, Western ; Chromatography, Affinity ; Electrophoresis, Polyacrylamide Gel ; Fibrinolysin ; analysis ; isolation & purification ; Humans ; Sepharose ; analogs & derivatives ; alpha-2-Antiplasmin ; analysis ; isolation & purification

OBJECTIVETo observe and compare the effects of Hanfangji Compound and IFN-gamma on expressions of transthyretin (TTR) , inter-alpha inhibitor H1 (ITIH1) and serpin peptidase inhibitor clade F member 2 (SERPINF2) of hepatic stellate cells (HSC-T6).

METHODHanfangji Compound and IFN-gammaof different concentrations were used in hepatic stellate cell-T6 (HSC-T6) for 48 h. Flow cytometer was used to detect the effects of Hanfangji Compound and IFN-gamma on HSC proliferation. RT-PCR method was adopted to detect mRNA expressions of TFR, ITIH1 and SERPINF2. TTR, ITIH1 and SERPINF2 secretions were detected by ELISA. The protein localizations of TTR, ITIH1 and SERPINF2 were examined by immune fluorescence. The protein expression of TfR and ITIHI were determined by Western blot.

RESULTAfter Hanfangji Compound and IFN-gamma were adopted in HSC-T6, compared with the control group, the cell proliferation was inhibited obviously (P < 0. 05) , protein expressions of TTR, ITIH1 and SERPINF2 and mRNA expression increased significantly, with certain correlation with concentrations of Hanfangji Compound. The 2. 5 g L-I Hanfangji Compound group was superior to the IFN-gamma group (P <0. 05).

CONCLUSIONHanfangji Compound can inhibit HSC proliferation, upregulated TTR, ITIH1 and SERPINF2 proteins and mRNA expression, which may be one of mechanisms of anti-hepatic fibrosis of Hanfangji Compound.

Alpha-Globulins ; genetics ; metabolism ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Enzyme-Linked Immunosorbent Assay ; Hepatic Stellate Cells ; cytology ; drug effects ; metabolism ; Humans ; Receptors, Albumin ; genetics ; metabolism ; alpha-2-Antiplasmin ; genetics ; metabolism

OBJECTIVEThe purpose of this work was to investigate the distribution pattern of fibrinolytic factors and their inhibitors in rabbit tissues.

METHODSThe components of the fibrinolytic system in extracts from a variety of rabbit tissues, including tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), plasminogen (Plg), plasmin (Pl) and alpha(2) plasmin inhibitor (alpha(2)PI), were determined by colorimetric assay.

RESULTSThe tissue extracts in renal, small intestine, lung, brain and spleen demonstrated strong fibrinolytic function, in which high activity of tPA, Plg and Pl was manifested; whereas in skeletal muscle, tongue and stomach, higher activity of PAI-1 and alpha(2)PI showed obviously. Also excellent linear correlations were found between levels of tPA and PAI-1, Pl and alpha(2)PI, Plg and Pl. In related tissues, renal cortex and renal marrow showed distinctly higher activity of tPA and lower activity of PAI-1, with the levels of Plg and Pl in renal cortex being higher than those in renal marrow, where the alpha(2)PI level was higher than that in renal cortex. Similarly, the levels of tPA, Plg and Pl in small intestine were higher than those in large intestine, but with respect to PAI-1 and alpha(2)PI, the matter was reverse. In addition, the fibrinolytic activity in muscle tissue was lower, however, the levels of tPA, Plg, and Pl in cardiac muscle were obviously higher than those in skeletal muscles, and the levels of PAI-1 and alpha(2)PI were significantly lower than those in skeletal muscle.

CONCLUSIONOur data demonstrate that a remarkable difference of the fibrinolytic patterns exists in rabbit tissues, which has probable profound significance in understanding the relationship between the function of haemostasis or thrombosis and the physiologic function in tissues.

Animals ; Female ; Fibrinolysin ; metabolism ; Fibrinolysis ; Gastric Mucosa ; metabolism ; Gastrointestinal Tract ; metabolism ; Intestinal Mucosa ; metabolism ; Male ; Organ Specificity ; Plasminogen ; metabolism ; Plasminogen Activator Inhibitor 1 ; metabolism ; Rabbits ; Tissue Extracts ; metabolism ; Tissue Plasminogen Activator ; metabolism ; alpha-2-Antiplasmin ; metabolism

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Apolipoproteins E ; blood ; genetics ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Venous Thromboembolism ; blood ; genetics ; Young Adult ; alpha-2-Antiplasmin ; analysis ; genetics

Certain natural anticoagulants are known to play critical roles on the control of hemostasis in addition to the physiologic role of fibrinolysis. Major antiproteases of this group include antithrombin III, protein C, protein S, alpha-2-antiplasmin, alpha-2-macroglobulin, etc. There has been increasing recognition of the importance of the control of coagulation and fibrinolysis, both by certain physiologic processes and by natural inhibitors. Especially, activated protein C (protein Ca) and its cofactor, protein S, now are recognized as significant modulators of fibrinolysis, thrombosis and hemostasis. Children and adults with decreased levels of either protein are at increased risk from thrombosis. We experienced a 5 year-old girl patient with cerebral infarction who initially presented with abnormal movement of left extremities. She had lacunar infarction in the posterior limb of the right internal capsule and hypoplastic left carotid artery on brain MRI and MR angiography. She was diagnosed to have protein S deficiency with the level of 43% in the screening test of hypercoagulable state. She remains clinically well after heparin and warfarin treatment with regular follow-up of prothrombin time. A brief review of the literature ensues with the case report.
Adult ; alpha-2-Antiplasmin ; Angiography ; Anticoagulants ; Antithrombin III ; Brain ; Carotid Arteries ; Cerebral Infarction* ; Child ; Child, Preschool ; Dyskinesias ; Extremities ; Female ; Fibrinolysis ; Follow-Up Studies ; Hemostasis ; Heparin ; Humans ; Internal Capsule ; Magnetic Resonance Imaging ; Mass Screening ; Protease Inhibitors ; Protein C ; Protein S Deficiency* ; Protein S* ; Prothrombin Time ; Stroke, Lacunar ; Thrombosis ; Warfarin