OBJECTIVETo explore the relationship between phlegm-stasis syndrome (PSS) and the fibrinolytic status in patients with non-alcoholic fatty liver (NAFL).

METHODSSeventy patients with NAFL were divided into the PSS group and non-PSS group according to TCM Syndrome typing, and a control group consisted of 28 healthy subjects was set up. Levels of plasminogen (PLG), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and D-dimer were determined and compared.

RESULTSThe activity of t-PA in NAFL patients was significantly lower than that in the control group (P<0.05), and PLG and PAI-1 were significantly higher than those in the control group (P<0.05). In respect to the TCM Syndrome typing, in patients of PSS, t-PA was significantly lower and PLG, PAI-1 were significantly higher than those in patients of non-PSS (P<0.05 or P<0.01), while D-dimer was insignificantly different between patients of the two Syndrome types (P>0.05).

CONCLUSIONNAFL patients of PSS type shows significant lower of fibrinolytic activity, indicating that there is certain degree of microcirculatory disturbance and hyper viscosity state, so the application of dissolving phlegm and dispelling stasis principle in treating NAFL is significant.

Adult ; Aged ; Diagnosis, Differential ; Fatty Liver ; blood ; diagnosis ; Female ; Fibrinolysis ; Humans ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Plasminogen ; metabolism ; Plasminogen Activator Inhibitor 1 ; blood ; Tissue Plasminogen Activator ; blood

OBJECTIVETo report a patient with congenital plasminogen activator inhibitor-1 (PAI-1) deficiency and explore its molecular mechanism.

METHODSThe activities of tissue plasminogen activator (tPA), alpha(2) antiplasmin (alpha(2)AP) and PAI-1 were measured by the methods of chromogenic substrate, the antigens of tPA and PAI-1 were measured by ELISA. PAI-1 gene was studied by PCR product sequencing and restriction endonuclease ana-lysing.

RESULTSIn the present patient, the euglobulin clot lysis time was 70 minutes and was corrected to normal range after added 50 ng/ml PAI-1 to his plasma. The activities of t-PA, alpha(2)AP, and factor were normal; the activity and antigen of PAI-1 in plasma were both significantly decreased. Nucleotide sequence analysis revealed that the patient had a heterozygous missense mutation in exon 2, a G to A transition at nucleotide 43. The possibility of gene polymorphism was excluded by restriction endonuclease analysing.

CONCLUSIONSIt is the first patient with congenital PAI-1 deficiency reported in China. The PAI-1 deficiency in the patient may be caused by compound heterozygosity, one of which is the G to A transition at nt43, a new mutation in congenital PAI-1 deficiency.

Adult ; Base Sequence ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Plasminogen Activator Inhibitor 1 ; blood ; deficiency ; genetics

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

OBJECTIVES: Plasma fibrinolytic activity is determined by the balance between plasmonogen activators and their inhibitors. The aim of this study was to compare the fibrinolytic activity before and after exercise of the type 2 diabetic patients with control group. METHODS: We measured plasma tissue-plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) antigen before and after standardized treadmill exercise in 21 type 2 diabetic patients (14 men, 11 women, ages 46.2+/-5.6 years) and 21 sex and age- matched control group (10 men, 11 women, ages 48.6+/-5.4 years). RESULTS: 1) Post exercise t-PA antigen increased in both diabetic group (from 7.36+/-3.89 to 10.62+/-4.81 ng/ml, p<0.05) and control group (from 8.30+/-3.99 to 10.99+/-5.52 ng/ml, p<0.05). But the rise in t-PA antigen with exercise was similar in both group. 2) Both base line and post exercise PAI-1 antigen levels were similar between the diabetic group (from 29.46+/-10.35 to 31.48+/-12.94 ng/ml, p>0.05) and control group (from 30.04+/-10.40 ng/ml to 31.06+/-10.88 ng/ml, p>0.05). 3) In diabetic group, significant correlations between base line PAI-1 antigen levels and serum triglyceride levels were observed. And post exercise PAI-1 antigen levels were correlated with systolic blood pressure. CONCLUSION: The results show that plasma t-PA antigen level is increased after vigorous exercise in patients with type 2 diabetes mellitus and plasma PAI-1 antigen level is not changed. The increment of plasma t-PA level is not different with healthy subjects.
Blood Pressure ; Diabetes Mellitus* ; Diabetes Mellitus, Type 2 ; Female ; Humans ; Male ; Plasma ; Plasminogen Activator Inhibitor 1* ; Plasminogen Activators ; Triglycerides

OBJECTIVETo study the protective impact of tea polyphenols (TP) on the injury of fibrinolytic functions induced by high-methionine dietary in rats.

METHODS50 male Wistar rats were divided by stratified based on body weight into 5 groups with 10 in each group: namely control group, model group, low-dose TP group, medium-dose TP group and high-dose TP group. The rats in model group and TP groups were fed with 3% methionine dietary, control group rats with routine diet. In addition, rats in low-dose, medium-dose and high-dose TP groups were treated with TP at 50, 100 and 200 mg/kg dosage respectively by gavages every day, control group and model group rats were given with same amount distilled water. The animals were sacrificed after 8 weeks. The levels of tissue-type plasminogen activator (t-PA) and type-1 plasminogen activator inhibitor (PAI-1) in plasma were determined by ELISA assays, mRNA levels of t-PA and PAI-1 in aortic arch were detected by RT-PCR, t-PA and PAI-1 expression in aortic arch were detected by immunohistochemistry strept-avidin-biotin complex (SABC).

RESULTSAfter experiment, the t-PA expression of aortic arch in control group, model group, low-dose TP group, medium-dose TP group and high-dose TP group were 133.03 ± 10.14, 95.46 ± 11.08, 111.97 ± 11.91, 130.23 ± 10.80, 139.39 ± 9.41 (F = 14.15, P < 0.01), respectively, and the PAI-1 expression were 90.91 ± 8.67, 166.76 ± 12.18, 139.63 ± 12.71, 134.66 ± 13.19, 109.49 ± 10.82 (F = 31.44, P < 0.01). The t-PA concentration of plasma were (10.69 ± 1.26), (6.13 ± 0.92), (8.56 ± 1.19), (9.69 ± 0.92), (11.97 ± 1.08) ng/ml, respectively (F = 41.98, P < 0.01), and the PAI-1 concentration of plasma were (6.31 ± 0.81), (16.98 ± 1.27), (11.39 ± 0.82), (8.46 ± 0.67), (8.08 ± 0.91) ng/ml, respectively (F = 207.74, P < 0.01). The mRNA levels of t-PA in aortic arch were 1.12 ± 0.02, 0.75 ± 0.14, 1.01 ± 0.09, 0.95 ± 0.08, 1.05 ± 0.13 (F = 5.77, P < 0.05), and the mRNA levels of PAI-1 in aortic arch were 1.25 ± 0.11, 1.74 ± 0.06, 1.23 ± 0.05, 1.09 ± 0.14, 1.23 ± 0.04 (F = 23.56, P < 0.01).

CONCLUSIONThe results indicate that TP seems to have regulatory function on transcription and protein levels of t-PA and PAI-1, in addition to maintaining the balance between PAI-1 and t-PA and healing the injury of fibrinolytic functions in rats induced by high-methionine dietary.

Animals ; Diet ; Fibrinolysis ; drug effects ; Male ; Methionine ; adverse effects ; Plasminogen Activator Inhibitor 1 ; blood ; Polyphenols ; pharmacology ; Rats ; Rats, Wistar ; Tea ; chemistry ; Tissue Plasminogen Activator ; blood

OBJECTIVESTo measure the plasma levels of urokinase plasminogen activator (uPA), urokinase plasminogen activator receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1), and study the relationship between the plasma levels of uPA, PAI-1 and the serum albumin (Alb), collagen type IV (CIV), the serum hyaluronic acid (HA), prothrombin time (PT) and prothrombin activity (PTA) in patients with different stages of liver cirrhosis following chronic hepatitis B.

METHODS72 cases with liver cirrhosis of different stages were classified according to child-pugh's categories A, B, C, in which there were 23 cases in child A, 29 cases in child B, and 20 cases in child C. The plasma levels of uPA, uPAR, PAI-1 and the serum levels of HA, CIV were detected by ELISA. The serum PCIII concentration was determined by radioimmunoassay.

RESULTSWith the progression of hepatic fibrosis, the plasma levels of uPA, uPAR and PAI-1 were (1.36+/-0.43) microg/L, (3.03+/-1.48) microg/L and (24.09+/-7.14) microg/L respectively in group A, (1.79+/-0.62) microg/L, (4.80+/-2.22) microg/L and (41.40+/-17.52) microg/L respectively in group B. The highest levels were in child C, whose levels were (1.88+/-0.64) microg/L, (4.82+/-2.02) microg/L and (52.60+/-16.87) microg/L respectively, compared with group A and group B, t value were from 2.81 to 7.38, all of P value were less than 0.01. There was negative correlation between the plasma levels of uPA and the serum PCIII (r=-0.4785, P<0.05) in child A, but, positive correlation between the plasma PAI-1 and the serum HA (r=0.5447, P<0.01) in child C. The value of PAI-1/uPA was significantly decreased in child A, but increased in child B and child C.

CONCLUSIONIn the late of liver cirrhosis, increased PAI-1 together with uPA, uPAR are associated with overall inhibition of matrix degradation. The plasma levels of uPA and PAI-1 were correlation to the progression of liver cirrhosis.

Female ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; blood ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1 ; blood ; Receptors, Cell Surface ; blood ; Receptors, Urokinase Plasminogen Activator ; Urokinase-Type Plasminogen Activator ; blood

Actins ; biosynthesis ; genetics ; Adult ; Aged ; Female ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; blood ; enzymology ; virology ; Male ; Matrix Metalloproteinase 1 ; biosynthesis ; genetics ; Middle Aged ; Plasminogen Activator Inhibitor 1 ; blood ; Tissue Inhibitor of Metalloproteinase-1 ; biosynthesis ; genetics ; Urokinase-Type Plasminogen Activator ; blood

OBJECTIVETo measure the concentration of D-dimer (DD), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen (PLG) activity in plasma and cerebrospinal fluid in patients with acute cerebral infarction and to investigate their clinical significance.

METHODSThe concentrations of D-dimer, t-PA, and PAI-1 in plasma and cerebrospinal fluid in patients were measured by enzyme-linked immunosorbent assay (ELISA). The PLG biological activity was detected using the chromophore method. The results were compared with those of the controls.

RESULTSThe concentrations of D-dimer, t-PA and PAI-1 in cerebrospinal fluid and plasma in patients with acute cerebral infarction were much higher than those of normal subjects (P < 0.01). Conversely, the level of PLG activity was significantly lower in the patients than in the controls (P < 0.01).

CONCLUSIONHypercoagulability and secondary hyperfibrinolysis exist in patients with acute cerebral infarction.

Acute Disease ; Aged ; Blood Coagulation ; Cerebral Infarction ; blood ; Female ; Fibrin Fibrinogen Degradation Products ; analysis ; cerebrospinal fluid ; Fibrinolysis ; Humans ; Male ; Middle Aged ; Plasminogen ; analysis ; cerebrospinal fluid ; Plasminogen Activator Inhibitor 1 ; blood ; cerebrospinal fluid ; Tissue Plasminogen Activator ; blood ; cerebrospinal fluid

OBJECTIVETo measure the plasma levels of transforming growth factor beta1 (TGFbeta1), the protein expression of alpha-SMA in hepatic stellate cells and urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1), and study on the relationships between the plasma levels of TGFbeta1, the protein expression and the serum hyaluronic acid (HA) in patients with different grades of hepatic fibrosis.

METHODSThirty seven cases with hepatic fibrosis of different grades were classified according to HE and VG staining categories from 0 to 4, in which there were 8 cases in grade 1, 9 cases in grade 2, 7 cases in grade 3, 13 cases in grade 4. The plasma levels of TGFbeta1 and the serum levels of HA were detected by ELISA. The protein expressions of a-SMA, uPA and PAI-1 in fibrotic liver tissue were observed by immunohistochemistry.

RESULTSWith the progression of hepatic fibrosis, the plasma levels of TGFbeta1 and the protein expression of a-SMA, uPA and PAI-1 in fibrotic liver tissue were increased. In grade 3 and 4, the plasma levels of TGFbeta and the protein expression of a-SMA and PAI-1 in fibrotic liver tissue were significantly increased, but the protein expression of uPA in cirrhosis liver tissue did not increased.

CONCLUSIONTGFbeta1, a-SMA, uPA and PAI-1 play an important role in the progression of hepatic fibrosis. Inhibiting the early activation of latent TGFbeta1 or increasing uPA and inhibiting PAI-1 over express may contribute to matrix degradation and retard the progression of hepatic fibrosis.

Actins ; blood ; Adult ; Aged ; Female ; Hepatitis B, Chronic ; blood ; complications ; Humans ; Liver Cirrhosis ; blood ; etiology ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1 ; blood ; Transforming Growth Factor beta ; blood ; Transforming Growth Factor beta1 ; Urokinase-Type Plasminogen Activator ; blood